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GIP (50 ng/mL) alone has no effect on PI hydrolysis. Paper-6121517.
The human GIP gene has been assigned to chromosome 17q21.3----q22. Paper-6370745.
Therefore, the solution structure of GIP in 50% TFE was determined. Paper-13258152.
Glucose-induced GIP levels in patients with insulinoma. Paper-4530817.
Pancreatic juice was considered to play a role in the secretion of GIP. Paper-15194844.
GIP is released from the precursor by processing at single arginine residues. Paper-5724381.
AA homozygotes had lower postprandial GIP concentrations than BB homozygotes. Paper-15314590.
No effect of gliclazide on gastric inhibitory polypeptide ( GIP) in type II diabetes. Paper-5624953.
Mannose ( C-2 epimer) which is passively absorbed by diffusion did not release GIP. Paper-4318383.
Recent studies in rodents suggested that GIP directly links overnutrition to obesity. Paper-13295742.
Insulin, enteroglucagon, neurotensin, and GIP rose significantly in all patients. Paper-4257666.
In contrast, insulin release did not occur with valine infused alone or with GIP. Paper-4521241.
Addition of glucomannan and soya-bean-cotyledon fibre did not affect circulating GIP levels. Paper-6506915.
Expression of ACTH receptor pathway genes in GIP-dependent Cushing's syndrome (CS). Paper-9604607.
GIP-dependent cAMP production with the 405 mutant was decreased in COS-7 cells. Paper-1990489.
Orlistat accelerates gastric emptying and attenuates GIP release in healthy subjects. Paper-13645741.
In the present study, we identified a novel role for GIP in regulating K(V)1.4 channel endocytosis. Paper-10784581.
Release of gastric inhibitory polypeptide ( GIP) during calcium infusion and in hyperparathyroidism. Paper-3993202.
The brain, bone, cardiovascular system, and gastrointestinal tract are additional targets of GIP. Paper-13643286.
This finding implies an endogenous insulin rhythm, whereas food intake controls GIP secretion. Paper-5861402.
With intravenous amino acid infusion, serum GIP concentrations remained below the assay detection limit. Paper-2636383.
Complementary DNA clones encoding human GIP were isolated from a library prepared with RNA from duodenum. Paper-5724381.
Bombesin and nutrients independently and additively regulate hormone release from GIP/Ins cells. Paper-10805830.
Both GIP and ACTH stimulated production of cAMP but not inositol 1,4,5-trisphosphate IP3). Paper-1781158.
There is also evidence of regulation of GIP secretion via neural pathways and somatostatin. Paper-15448518.
In this study we report the presence of insulin and GIP in human AF of normal and diabetic pregnancies. Paper-5066320.
GIP and hCG stimulated cortisol production via activation of cAMP-dependent protein kinase A in H2. Paper-12305143.
Arachidonic acid is therefore a new component of GIP-mediated signal transduction in the beta-cell. Paper-8996926.
Here we demonstrate that bombesin and nutrients additively stimulate hormone release from GIP/Ins cells. Paper-10805830.
Glutamine also increased plasma GIP concentrations but less effectively than glucose. Paper-13565829.
Sorbitol (reduced alcohol of glucose) which is not absorbed did not release GIP. Paper-4318383.
GIP did not affect aldosterone and cyclic-AMP release by dispersed zona glomerulosa cells. Paper-8307973.
Glucose-dependent insulinotropic polypeptide stimulates the proliferation of colorectal cancer cells. Paper-15216308.
In adipose tissue, GIP interacts with insulin to increase lipoprotein lipase activity and lipogenesis. Paper-13643286.
Enteroglucagon and GIP after oral glucose in patients with prolactinoma and acromegaly. Paper-4517340.
The human gene coding for the human GIP precursor spans approximately 10 kilobase pairs and consists of six exons. Paper-6370745.
The in vitro secretory response to GIP was higher for the adrenal androgen DHEA, compared with cortisol. Paper-8676525.
We sought to determine whether GIP also might be co-expressed with proglucagon in pancreatic alpha-cells. Paper-15066805.
Cortisol production by cultured adrenal adenoma cells from the patient was stimulated by GIP and ACTH. Paper-663509.
GIP also has an effect on the volume and/or electrolyte composition of intestinal secretion and saliva. Paper-6226850.
The data suggests that postprandial insulin and GIP responses are key players in short-term appetite regulation. Paper-8919186.
GIP and insulin responses to oral glucose in coeliac patients before and after treatment. Paper-11979691.
Thyroidectomy-induced hypothyroidism increased the basal level of plasma GIP, but decreased that of insulin. Paper-885995.
The response of gastric inhibitory polypeptide ( GIP) to ethanol was very slight, similar to that of insulin. Paper-5089324.
GIP immunoreactive cells were observed in the pancreas of five foetuses with gestational ages of 18-20 weeks. Paper-3987733.
GLP concentrations remained high throughout lactation but those of GIP declined linearly as milk yields fell. Paper-1538345.
Interestingly, the GIP promoter activity was repressed by the c-jun proto-oncogene product, possibly through the CREs. Paper-7571970.
GIP receptor localization in the adrenal cortex suggests that it may have effects on glucocorticoid metabolism. Paper-7631130.
Actively transported galactose ( C-4 epimer) stimulated GIP release, but less than glucose. Paper-4318383.
We have demonstrated the possibility that GIP stimulates GH secretions from the pituitary adenoma cells of acromegalics. Paper-10172995.
Bombesin-like peptides produced by enteric neurons and luminal nutrients stimulate GIP release in vivo. Paper-10805830.
GIP has extrapancreatic actions on adipogenesis, neural progenitor cell proliferation, and bone metabolism. Paper-15448518.
These findings demonstrate that the GIP receptor is linked to the MAP kinase cascade via at least two different pathways. Paper-1065992.
GIP can be considered as a true metabolic hormone, with most of its functions tending to increase anabolism. Paper-6226850.
Plasma GIP increased following the glucose or galactose load to 4360 or 1653 pg/ml, respectively. Paper-4519440.
Ubiquitination is involved in glucose-mediated downregulation of GIP receptors in islets. Paper-13364610.
These results suggest that thyroid functions are involved in the regulation of insulin and GIP secretion in rats. Paper-885995.
Epinephrine alone and epinephrine + phentolamine did not influence glucose-stimulated GIP. Paper-3985345.
There appears to be no direct effect of the autonomic nervous system on glucose-induced secretion of GIP. Paper-5184771.
Higher doses of GIP significantly potentiated insulin release stimulated by glucose or arginine. Paper-3979472.
Reversal of impaired GIP and insulin secretion in patients with pancreatogenic steatorrhea following enzyme substitution. Paper-3701422.
The GIP moiety is flanked by polypeptide segments of 51 and 60 amino acids at its NH2 and COOH termini, respectively. Paper-5724381.
The concentrations of plasma GIP, insulin and triiodothyronine (T3) were measured by specific radioimmunoassays. Paper-7594207.
High-carbohydrate, low-fat diet: effect on lipid and carbohydrate metabolism, GIP and insulin secretion in diabetics. Paper-4836318.
Competitive-binding displacement studies indicated that these peptides were low-affinity ligands for the GIP receptor. Paper-8797114.
The predicted amino acid sequence indicates that GIP is derived by proteolytic processing of a 153-residue precursor, preproGIP. Paper-5724381.
The response of gastric inhibitory polypeptide ( GIP) and insulin to glucose in duodenal ulcer patients. Paper-2949530.
Independent of the discovery of GIP, the K-cell was identified in small intestine by characteristic ultrastructural features. Paper-15448518.
Circadian rhythms occurred for insulin with all feeding schedules and for GIP with all schedules except fasted rats. Paper-5861402.
The effect of dietary modification and hyperglycaemia on gastric emptying and gastric inhibitory polypeptide ( GIP) secretion. Paper-5916235.
Our data suggest the contribution of altered GIP secretion in the pathogenesis of hyperinsulinemia in essential hypertension. Paper-242220.
Molecular cloning, functional expression, and signal transduction of the GIP-receptor cloned from a human insulinoma. Paper-385856.
Insulin-dependent inhibition of hepatic glycogenolysis by gastric inhibitory polypeptide ( GIP) in perfused rat liver. Paper-5171124.
GIP mRNA could be detected as early as day 20 of embryonic development and very low levels remained until postnatal day 3. Paper-8047770.
These results suggest the possibility that the adrenergic nervous system may have a role in the regulation of GIP secretion in man. Paper-3985345.
Furthermore, the GIP receptor appears to play a role in facilitating glucose uptake in the small intestine. Paper-1917103.
The present data represents the first analysis of functionally relevant GIP binding sites in a insulin-secreting cell. Paper-4909846.
GIP powerfully inhibited pentagastrin-stimulated acid secretion from the Heidenhain pouch but not from the gastric fistula. Paper-4725810.
In conclusion, mutations or SNPs in the regulatory region of the GIPR gene are unlikely to underlie GIP-dependent CS. Paper-10474783.
GIP fragments produced by cleavage with cyanogen bromide and trypsin showed no significant stimulation of IRI release. Paper-2244813.
Mannitol and glucose: effects on gastric acid secretion and endogenous gastric inhibitory polypeptide ( GIP). Paper-2967022.
The interaction of GIP with its receptors in the hamster pancreatic insulin-secreting beta cell line, In lll, has been analyzed. Paper-4909846.
Diurnal GIP, PP and insulin levels in morbid obesity before and after stapled gastric partitioning with gastro-gastrostomy. Paper-4542025.
We conclude that food-dependent Cushing's syndrome results from the expression of GIP receptors on adrenocortical adenoma cells. Paper-663509.
Plasma GIP levels were also increased significantly, 24% with terbutaline at 10 micrograms/kg/hr, and 39% at 20 micrograms/kg/hr. Paper-6793711.
However, amylin failed to modify GIP-induced insulin release in pancreata obtained from pertussis toxin pretreated rats. Paper-8214427.
At 10(-7) and 10(-6) mol/l, calcitonin and GIP reduced the response to histamine by 10-20% following noncompetitive kinetics. Paper-5089259.
CONCLUSION: These studies exclude both GIP and GLP-1 as key mediators for the immediate reduction in bone resorption seen after a meal. Paper-10199022.
Tests of antibody specificity showed that the GIP antiserum did not cross-react with either pancreatic- or gut-type glucagon. Paper-4525848.
Active immunization with glucose-dependent insulinotropic polypeptide vaccine influences brain function and behaviour in rats. Paper-15274760.
This study demonstrates the molecular cloning of a cDNA for the GIP-receptor from a human insulinoma lambda gt11 cDNA library. Paper-385856.
GIP treatment reduced glucolipotoxicity-induced cell death in C57 BL/6 and Bax(-/-) islets, but not GIPR(-/-) mouse islets. Paper-10742543.
Nocloprost was without effect on gastric inhibitory polypeptide ( GIP) and did not influence insulin or C-peptide concentrations. Paper-6179692.
Using the lymph fistula rat model to study the potentiation of GIP secretion by the ingestion of fat and glucose. Paper-14422620.
High levels of GIP immunoreactivity were observed in the olfactory bulb, hippocampus, and Purkinje cells in the cerebellum. Paper-13339322.
Effects of hormones (calcitonin, GIP) and pharmacological antagonists ( ranitidine and famotidine) on isolated rat parietal cells. Paper-5089259.
Glucose-dependent insulinotropic polypeptide is expressed in pancreatic islet alpha-cells and promotes insulin secretion. Paper-15066805.
Finally, food deprivation studies in larvae demonstrated an increase in GIP and proglucagon II mRNA levels in response to fasting. Paper-14585073.
A role for GIP in the regulation of lipid homeostasis and in the development of obesity has been inferred from different animal studies. Paper-10628667.
Following incubation in plasma, (Ser2)GIP had a reduced hydrolysis rate compared with native GIP, while (Gly2)GIP was completely stable. Paper-9707514.
Oral administration of glycerol (1 g/kg) slightly elevated the blood glucose levels but not the plasma GIP. Paper-4804661.
However, sub-chronic passive GIP immunisation was not associated with any changes in body weight, food intake or metabolic control. Paper-13497077.
Background infusion of bethanechol totally abolished the inhibitory action of GIP in both the Heidenhain pouch and gastric fistula. Paper-4725810.
Elevated plasma glucose-dependent insulinotropic polypeptide associates with hyperinsulinemia in impaired glucose tolerance. Paper-10464072.
Since GIP is being implemented in the development of obesity, its role in weight control attained by orlistat awaits further investigation. Paper-13645741.
RESULTS: The addition of 1 or 3 g cinnamon had no significant effect on GER, satiety, glucose, GIP, or the ghrelin response. Paper-13624436.
Insulin and gastric inhibitory polypeptide ( GIP) have a circadian rhythm of secretion that is altered by various feeding schedules. Paper-5861402.
Receptor gene expression of glucagon-like peptide-1, but not glucose-dependent insulinotropic polypeptide, in rat nodose ganglion cells. Paper-10406513.
Glucose-dependent insulinotropic polypeptide may enhance fatty acid re-esterification in subcutaneous abdominal adipose tissue in lean humans. Paper-15380954.
There is increasing realization that gastric inhibitory polypeptide ( GIP) has actions outside of the pancreas and gastrointestinal tract. Paper-12946103.
These data indicate that changes in the secretion and actions of GIP may be involved in the metabolic adaptations to cold acclimation in rats. Paper-15693968.
These studies indicate that the presence of GIP receptors in CRC may enable ligand binding and, in so doing, stimulate CRC cell proliferation. Paper-15216308.
Remarkably, high glucose leads to an increase in the same intracellular signals, as does a combination of acetylcholine and GIP. Paper-12669.
The magnitude of the increase in plasma GIP after oral glucose load was positively correlated to the length of residual jejunum. Paper-3449790.
However, cortisol secretion occurs in response to gastric inhibitory polypeptide ( GIP) in rare cases of food-dependent Cushing's syndrome (CS). Paper-11124257.
ZDF rats with extreme hyperglycemia demonstrated greater islet GIP receptor mRNA down-regulation (94.3+/-3.8%) than ZF rats (48.8+/-22.8%). Paper-12497127.
Both proglucagon and GIP were found to be single-copy genes in mammals, and exist in stable genomic neighborhoods with conserved flanking gene order. Paper-13816403.
Glucose-dependent insulinotropic polypeptide enhances adipocyte development and glucose uptake in part through Akt activation. Paper-12630473.
On the other hand, GIP secretion was blunted after the operation only in diabetic patients, suggesting a role in insulin resistance and diabetes. Paper-13702761.
The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients. Paper-10991982.
When expressed in Chinese hamster lung fibroblasts, both forms of the receptor displayed high-affinity binding for GIP (180 and 600 pmol/l). Paper-357812.
In xylitol adapted rats it did not cause diarrhoea but still had no effect upon GIP release in contrast to glucose, which did. Paper-3985442.
It would appear that structurally similar receptors exist for both the active transport of glucose and for the release of GIP. Paper-4318383.
Both methionine- and leucine-enkephalins caused a dose-dependent inhibition of gastric inhibitory polypeptide ( GIP) stimulated SLI secretion. Paper-4437445.
Lack of a direct effect of the autonomic nervous system on glucose-stimulated gastric inhibitory polypeptide ( GIP) secretion in man. Paper-5184771.
Thus, in NIDDM subjects, glucose and insulin responses to different mixed meals do not appear to be exclusively mediated by GIP. Paper-6864000.
The effect of thyroid hormones on glucose-induced secretion of gastric inhibitory polypeptide ( GIP) and insulin was studied. Paper-885995.
The glucose-dependent insulinotropic polypeptide and glucose-stimulated insulin response to exercise training and diet in obesity. Paper-13804529.
This appears to be the first demonstration of a GIP-stimulated signal transduction pathway involved in increasing fat storage in adipocytes. Paper-12459872.
At the dose of 5 ng/ml used for both GIP preparations, only GIP-EG III significantly stimulated volume and amylase secretion of the exocrine pancreas. Paper-4272674.
BACKGROUND/AIMS: Gastric inhibitory polypeptide is recognized as an acid inhibitor, while its relationship with Helicobacter pylori colonization is unknown. Paper-1980053.
Serum insulin concentrations correlated positively with plasma glucose concentrations but not with either GIP or GLP concentrations. Paper-1538345.
GAS, GIP and GLU-IR endocrine cells were found in the intestinal mucosa of silver carp, bighead, silver crucian carp and bluntnose black bream. Paper-15030893.
Five patients after ileoascendostomia for familial hypercholesterolemia had significantly supernormal GIP release during OGTT but normal incretin effect. Paper-3443029.
Serum gastric inhibitory polypeptide ( GIP) in duodenal ulcer disease: relationship to glucose tolerance, insulin, and gastrin release. Paper-3054943.
The effects of gastric inhibitory polypeptide ( GIP) on glucose and lipid metabolism of isolated rat adipocytes were investigated. Paper-6084346.
Oral administration of tricaprylin (2 g/kg) did not elicit any discernible changes in the blood glucose nor in the plasma GIP. Paper-4804661.
Gastrointestinal peptides and neoplasia ectopic gastric inhibitory polypeptide ( GIP) receptors in adrenal glands causing food-dependent Cushing's syndrome. Paper-12778593.
At 30 min, however, IRI and GIP were higher in normotensives with a family history of hypertension and in established hypertensive versus control subjects. Paper-242220.
Aging and obesity are characterized by decreased beta-cell sensitivity and defects in the potentiation of nutrient-stimulated insulin secretion by GIP. Paper-13804529.
The promoter region of the human GIP gene contains potential binding sites for a number of transcriptional factors including Sp 1, AP-1, and AP-2. Paper-6370745.
Treatment with octreotide initially prevented the meal-induced increases in cortisol and GIP levels and decreased urinary cortisol excretion. Paper-663509.
Taken together, our results suggest that the proximal intronic sequences contain essential cis-acting elements for the cell-specific expression of the hGIP gene. Paper-15202939.
Glucose-dependent insulinotropic polypeptide activates the Raf-Mek1/2-ERK1/2 module via a cyclic AMP/ cAMP-dependent protein kinase/Rap1-mediated pathway. Paper-9171512.
In COS-7 cells transiently transfected with the human GIP receptor, GIP-(1-42) and -(3-42) bind with affinities (IC(50)) of 5.2 and 22 nM, respectively. Paper-12178766.
In the present study we identified Forkhead (Foxo1)-mediated suppression of the bax gene as a critical component of the effects of GIP on cell survival. Paper-10742543.
GIP-infusion resulted in circulating insulin concentration of 1109+/-942 pmol/l (p<0.02) and no further decrease of ghrelin (86.2% of baseline, p=0.050). Paper-11220214.
And we also revealed some genetic events in the early stage of diabetic retinopathy including the de novo increment of GIP and GIPR expression in the retina. Paper-10684750.
While GIP strongly stimulates insulin release in healthy humans, the peptide has almost completely lost its insulinotropic effect in patients with type 2 diabetes. Paper-10628667.
Total integrated GIP ( P < 0.05) and glucose ( P < 0.01) responses were higher post heparin than after acipimox in obese subjects only. Paper-1812126.
High saturated-fat diet induces apoptosis in rat enterocytes and blunts GIP and insulin-secretive response to oral glucose load. Paper-12765489.
This effect is not due to diversion of portal blood to the systemic circulation and may be attributable to hypersensitivity of the alpha-cells to stimulation by GIP. Paper-6865271.
RESULTS: To determine whether GIP and GIPR are important components in adipocyte development, the expression profile of GIPR during differentiation was examined. Paper-12630473.
METHODS: We assessed GIP expression via reverse-transcription polymerase chain reaction, in situ hybridization, and immunohistochemistry. Paper-15066805.
GIP acted synergistically with insulin to increase neutral lipid accumulation during progression of 3T3-L1 preadipocytes to the adipocyte phenotype. Paper-15761807.
GIP was nonlipolytic and inhibited lipolysis stimulated by glucagon but not that stimulated by secretin or vasoactive intestinal polypeptide ( VIP). Paper-2658503.
We defined the exon-intron boundaries of the human GIP receptor, made a mutational analysis of the gene and identified two amino acid substitutions, A207 V and E354Q. Paper-1680481.
It is concluded that porcine GIP is glucagonotropic in patients with cirrhosis of the liver who show elevated levels of IRG in the plasma in the postabsorptive state. Paper-6865271.
Improved pancreatic beta-cell function in type 2 diabetic patients after lifestyle-induced weight loss is related to glucose-dependent insulinotropic polypeptide. Paper-15182561.
GIP receptors are present in the ZF/ R of the normal adrenals, and are particularly abundant in some types of adrenocortical adenomas and hyperplasias. Paper-8498144.
No significant difference in the allele frequency and genotype distribution of any of the SNPs in GIP were observed between cases and controls ( P > 0.05). Paper-15361815.
Frequent blood samples were obtained over 6 h to determine plasma GIP, GLP-1, glucose, insulin, glucagon, resistin, and acetaminophen levels. Paper-13799562.
When given an oral fat load (1 ml triolein) plasma gastric inhibitory polypeptide ( GIP) and triglyceride levels were significantly higher in the fat pretreated group. Paper-4518744.
Expression of G5 in bacteria generated immunopositive GIP together with GFP fluorescence, while G4 generated only fluorescence without immunoreactivity. Paper-8785496.
Plasma GIP responses after the meal on the days with ranitidine alone or together with the gastrin infusion did not differ significantly from that found on the control day. Paper-4082300.
Furthermore, after the intervention, changes in insulin (DeltaI(0-30)/DeltaG(0-30)) and GIP (Delta(0-30)) secretion were correlated ( r = 0.69, P = 0.05). Paper-13804529.
This insensitivity of the diabetic B-cells towards incretins can be overcome by supraphysiological (pharmacological) concentrations of GLP-1 [7-36], however not of GIP. Paper-8861481.
During the oGTT, plasma GIP concentrations rose from 92 +/- 18 pmol 1(-1) to 257 +/- 42 pmol 1(-1) 60 min after ingestion of glucose (mean +/- SEM). Paper-6564400.
The glucose-dependent action of GIP on pancreatic beta-cells has attracted attention towards its exploitation as a potential drug for type 2 diabetes. Paper-11434786.
MATERIALS AND METHODS: On separate occasions we performed an OGTT and administered an i.v. bolus of 20 pmol GIP/kg body weight in 20 women with pGDM and 20 control women. Paper-11074954.
Following oral glucose, morphine slowed gastric emptying and reduced plasma concentrations of glucose, insulin, and GIP. Paper-5167492.
The signal transduction pathways of a cloned human gastric inhibitory polypeptide ( GIP) receptor have been investigated in CHO cells stably expressing this receptor. Paper-1065992.
These data suggested that some somatotroph adenoma cells have an aberrant response to GIP which may go toward explaining paradoxical GH secretions to OGTT in acromegalics. Paper-10172995.
Proteinase K digestion and immunocytochemical studies on mutant K(V)1.4 localization following GIP stimulation demonstrated phosphorylation-dependent rapid endocytosis of K(V)1. Paper-10784581.
Palmitate (1 g/kg) administration did not change the blood glucose whereas the plasma GIP was increased remarkably and remained elevated at 120 min. Paper-4804661.
Treatment of VDF rats with a DP IV inhibitor ( P32/98) resulted in improved glucose tolerance and restored sensitivity to GIP in isolated pancreata. Paper-12497127.
In obese subjects with glucose intolerance i.v. glucose completely failed to lower the exaggerated secretion of IR- GIP following oral fat. Paper-3385492.
Plasma glucose, serum insulin ( IRI), and GIP were evaluated after a mixed meal containing a total of 82 g of carbohydrates, and 2 g sodium chloride. Paper-242220.
Chronic treatment of Vancouver diabetic fatty Zucker rats with GIP resulted in down-regulation of Bax and up-regulation of Bcl-2 in pancreatic beta-cells. Paper-10742543.
GIP1-42 is a substrate of the circulating enzyme dipeptidyl peptidase IV, which removes the N-terminal peptide Tyr-Ala resulting in the inactive polypeptide GIP3-42. Paper-10721162.
There is a region of nine amino acids in the COOH-terminal propeptide of the GIP precursor that has partial homology with a portion of chromogranin A as well as pancreastatin. Paper-5724381.
Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. Paper-2678533.
Effects of aging on the secretion of gastric acid and the response of gastric inhibitory polypeptide ( GIP) and insulin after oral glucose were studied. Paper-7594207.
The expression of the GIP receptor in tumor cells, but not in the adjacent normal adrenal, was demonstrated by RT-PCR), using specific oligonucleotide probes for this receptor. Paper-8676525.
Influence of breakfasts with different nutrient contents on glucose, C peptide, insulin, glucagon, triglycerides, and GIP in non-insulin-dependent diabetics. Paper-6864000.
CCK-8, CCK-33, and GIP (100 pmol/kg) all potentiated the meal-induced plasma responses of insulin and PP, whereas plasma levels of glucagon after the meal were not affected. Paper-7005206.
Using a hamster derived clonal beta-cell line, the HIT-T15 cell, wortmannin inhibited GIP-stimulated insulin secretion under both static incubation and perfusion conditions. Paper-605325.
In conclusion, independent of its insulinotropic action, GIP showed a insulin-like activity on glucose metabolism and lipolysis in rat adipose tissue. Paper-6084346.
Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide ( GIP) release occurred following glucose ingestion. Paper-4995792.
A single type of cell showing round, homogeneous, fairly osmiophilic granules with closely applied membrane and a mean size of 188 nm +/- 34 SD has been identified as the GIP cell. Paper-4817655.
The first feed of human milk caused a rise in blood glucose and plasma insulin, gastrin and enteroglucagon, but no change occurred in GIP or pancreatic glucagon. Paper-3215623.
However, the ectopic expression of GIP and V(2) receptor proteins in tumorous zona fasciculata tissue may play a role in the pathogenesis of canine cortisol-secreting ATs. Paper-15188620.
Phylogenetic analysis of the glucagon-like ligands suggested proglucagon as the common ancestor, supporting the theory that GIP arose as a gene duplication of proglucagon. Paper-16164011.
GIP (10(-7) M) did not display any additive or potentiating effect on corticosterone and cyclic-AMP responses to submaximal or maximal effective concentrations of ACTH. Paper-8307973.
Diffuse pancreatic islet cell hyperplasia was present and, although GIP was unmeasureable in the pancreas of normal subjects, it was at least 83 ng/g wet weight in this patient. Paper-3433539.
METHODS: Ten healthy subjects (9 men, 1 woman; age 33+/-11; BMI 26.8+/-2.2 kg/m(2)) received three different doses of intravenous GIP (7, 20, and 60 pmol/kg body weight) and placebo. Paper-9923797.
Moreover, GIP alone induced the transcription of c-jun mRNA; however, in combination with IL-6, it stimulated de novo synthesis of DNA and the transcription of both c-jun and c-fos genes. Paper-7922230.
Therefore, we studied the insulinotropic effect of GIP in women with previous gestational diabetes (pGDM) under euglycaemic fasting conditions and during a hyperglycaemic clamp experiment. Paper-11074954.
4. Expression of K(V)1.4 protein was also demonstrated in human beta-cells; GIP treatment resulting in similar decreases in A-type potassium current peak amplitude to those in HEK293 cells. Paper-10784581.
Identification of two missense mutations in the GIP receptor gene: a functional study and association analysis with NIDDM: no evidence of association with Japanese NIDDM subjects. Paper-782046.
GIP also promotes energy storage via direct actions on adipose tissue, and enhances bone formation via stimulation of osteoblast proliferation and inhibition of apoptosis. Paper-13234127.
Mannose, 6-deoxygalactose, 2-deoxyglucose, myoinositol, fructose or lactose (100 mmol/l of each) did not stimulate GIP release compared with controls. Paper-3580374.
However, BFA significantly reduced the upregulation induced by lumenal glucose and vascular GIP and blocked the stimulation produced by vascular GLP-2. Paper-1667351.
A steroidogenic secretory pattern, indicating the concomitant release of adrenal androgens and cortisol, was also observed in vitro from tumor cells cultured in the presence of GIP. Paper-8676525.
In contrast, adrenal cells from normal adults and fetuses or patients with cortisol-producting or aldosterone-producing adenomas responded to corticotropin but not to GIP. Paper-7259932.
The hyperinsulinism of morbid obesity and its amelioration after gastric bypass may be caused by markedly elevated levels of GIP before surgery and its reduced release after bypass. Paper-5189355.
The current report examines the N-terminal bioactive domain of GIP residing in residues 1-14 by alanine scanning mutagenesis and N-terminal substitution/modification. Paper-10530052.
However, eliminating the effect of endogenous GIP may at the same time impair postprandial insulin secretion, thereby severely disturbing glucose homeostasis. Paper-11580824.
The present study examined the ability of NH2-terminal modification of human GIP to protect from plasma degradation and enhance insulin-releasing and antihyperglycemic activity. Paper-1791957.
In this study, we addressed the role of glucose concentration in the diabetic range of >or=11 mM, i.e., hyperglycemia per se, as a cause of the lack of response to GIP. Paper-13364610.
In addition to its insulinotropic activity, GIP exerts a number of additional actions including promotion of growth and survival of the pancreatic beta-cell and stimulation of adipogenesis. Paper-13643286.
These results suggest that GIP response to oral glucose loading is enhanced in diabetic patients in proportion to the degree of their glucose intolerance. Paper-3754899.
A hyperbola-like relationship was found between the degree of insulin sensitivity (Matsuda index) and the insulin secretory response to GIP and i.v. glucose administration. Paper-11074954.
Fifty grams of each triglyceride rich fat were ingested and serum cholesterol, triglyceride, glucose, insulin, and GIP levels were determined over a 180-minute period. Paper-5963538.
To assess the possible role of the GIP receptor gene in genetic susceptibility to NIDDM, we have examined the allelic frequencies of Gly198Cys and Glu354Gln in NIDDM and control subjects. Paper-782046.
At the higher dose level the stimulated secretory rate declined throughout the perfusion suggesting that secretion exceeded the capacity to synthesize SLI under excessive GIP stimulation. Paper-3914382.
GIP and its receptor present a widespread distribution in the mammalian brain where they have been implicated with synaptic plasticity, neurogenesis, neuroprotection and behavioral alterations. Paper-15367591.
OBJECTIVE: We assessed GIP response to SFA ingestion and its effect on glucose and lipid metabolism and on liver injury in patients with nonalcoholic steatohepatitis (NASH). Paper-13578622.
Research on the defective incretin action in type 2 diabetes mellitus suggests that the observed loss of insulinotropic activity may be due primarily to a decreased responsiveness of β-cells to GIP. Paper-15601886.
Our results suggest that in obese subjects compensatory secretion of GIP was incomplete and could not prevent impairment in glucose tolerance after heparin-induced rise in NEFAs. Paper-1812126.
Treatment of INS-1(832/13) beta-cells with GIP resulted in concentration-dependent activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB)/Foxo1 signaling module. Paper-10742543.
Addition of 5 mmol phloridzin/l to a perfusate containing 50 mmol glucose/l prevented intestinal absorption of glucose and abolished the GIP response. Paper-3580374.
We studied the effects of orally or intraperitoneally administrated misoprostol on rat gastric emptying and looked what was the role of gastric inhibitory polypeptide ( GIP) in this emptying. Paper-1822971.
In comparison, GIP concentrations in acid ethanol extracts of the small intestine were significantly higher during suckling and GLP-1(7-36)amide concentrations significantly higher after weaning. Paper-689482.
Using mutant forms of K(V)1.4 with Ala-Ser/Thr substitutions in a potential PKA phosphorylation site, C-terminal phosphorylation was shown to be linked to GIP-mediated current amplitude decreases. Paper-10784581.
It is suggested that the glucose-induced GIP release into the portal vein mainly is effected first after glucose has gained access inside the mucosal cells. Paper-3849437.
Serial insulin ( IRI) and gastric inhibitory polypeptide ( GIP) levels were measured as well as the level of glucose infusion necessary to maintain the stable hyperglycemic level. Paper-4243305.
From these studies, we now know that GIP not only mediates early insulin secretion by acting on pancreatic beta-cells, but also links overnutrition to obesity by acting on adipocytes. Paper-11580810.
Alanine scan studies of these N-terminal residues showed that the GIP-(1-42)Ala(6) was the only analogue to show insulin-secreting activity similar to that of the native GIP. Paper-12034060.
In the isolated perfused rat pancreas, GIP-(3-42) alone had no effect on insulin output and only reduced the response to GIP (1 nM) when coinfused in >50-fold molar excess (IC(50), 138 nM). Paper-12178766.
Amylin inhibited the insulin response to glucagon (approx. 70%), GIP (approx. 90%), IBMX (approx. 75%) as well as the early phase of forskolin-induced insulin output (approx. 74%). Paper-8214427.
A high saturated-fat diet stimulates GIP secretion but with time induces apoptosis of duodenal villi epithelium, showing for the first time that enterocytes are also prone to lipoapoptosis. Paper-12765489.
In patients with chronic pancreatitis improvement of pancreatogenic insufficiency reverses the impaired GIP response, restores the incretin effect of fat, and improves glucose tolerance. Paper-3701422.
Transfection of NIH3T3 cells with cDNAs of G1, G3, G5, but not G2, G4, and EGFP, resulted in immunologically detectable GIP formation, although fluorescence could be detected in the latter two. Paper-8785496.
Compared to all other treatments, caffeinated and decaffeinated coffee produced higher GLP-1a response at 6.25 h ( P < 0.05), whereas only caffeinated coffee increased GIP secretion ( P < 0.05). Paper-15755940.
The ingestion of glucose or galactose resulted in a similar increment of GIP ( P less than 0.01), followed by a similar increment in the IRI response to iv glucose. Paper-3205496.
RESEARCH METHODS AND PROCEDURES: Isolated rat adipocytes were perifused on a column with 10 nM GIP alone or in combination with 10 microU/mL insulin, 1 microM isoproterenol, or 1 microM ANTGIP. Paper-12170766.
Insulin and GIP caused a significantly greater stimulation of [14C]acetate incorporation into fatty acids in omental adipose tissue than in either epididymal or subcutaneous adipose tissue. Paper-42536.
We conclude that the postprandial release of GIP and somatostatin increases and that the release of gastrin decreases when the intestinal mucosa is regenerated in celiacs on a gluten-free diet. Paper-4439274.
The half-life of both in plasma was determined by intravenous injection of GIP or GLP-1 in both dry and lactating animals, but neither peptide showed a significantly different value during lactation. Paper-1331302.
In this study, we found that jejunal reduction of the GIP gene by feeding normal rats dietary RS was associated with decreases in histone H3 and H4 acetylation on the promoter/enhancer region of the gene. Paper-14621793.
CCK-8, CCK-33, and GIP were all found to increase the basal plasma levels of insulin, somatostatin, and PP; the increases were observed already in samples taken at 2 min after the injection. Paper-7005206.
CONCLUSIONS/INTERPRETATION: These results do not support the hypothesis of an early defect in GIP action as a risk factor for subsequent development of diabetes in women with previous gestational diabetes. Paper-11074954.
GIP receptor mRNA is present in the pancreas as well as the gut, adipose tissue, heart, pituitary, and inner layers of the adrenal cortex, whereas it is not found in kidney, spleen, or liver. Paper-7631130.
In healthy human subjects xylitol taken by mouth in solution as a single 30 g dose produced only a minimal rise in blood glucose and no rise in plasma GIP or insulin concentration. Paper-3985442.
The molecular configuration of monosaccharides which have the ability to stimulate GIP release agreed well with the structural requirements for active transport by the sodium-dependent hexose pathway. Paper-3580374.
In this study we investigated whether CCK-33 and VIP could influence the insulinogenic effect of simultaneously administered GIP and 6.7 mmol/l glucose in the perfused rat pancreas. Paper-6128308.
Compared with preoperative values, fasting concentrations and integrated incremental areas for glucose, insulin, and GIP were decreased after a 25% weight loss after gastric bypass. Paper-5189355.
Cells containing immunoreactive GIP were confined to the mucosa of the duodenum, jejunum and ileum and were not observed in the forestomachs, abomasum, large intestine and pancreas. Paper-5259590.
Venous blood samples were taken before, and at intervals for 180 min following the meal, and analysed for insulin, gastric inhibitory polypeptide ( GIP) and paracetamol (as an index of gastric emptying). Paper-6506915.
We conclude that in man, both CCK-8, CCK-33, and GIP moderately stimulate basal and meal related insulin release without any synergistic effects and that the peptides do not inhibit the secretion of glucagon. Paper-7005206.
Plasma concentrations of glucagon-like peptide-1(7-36)amide ( GLP) and gastric inhibitory polypeptide ( GIP) were determined at fortnightly intervals for over a year throughout the pregnancy-lactation cycle of goats. Paper-1538345.
CCK-8 and GIP together (100 pmol/kg for both) increased plasma levels of insulin, PP and somatostatin as much as each of the peptides given alone, both under basal conditions and after the meal intake. Paper-7005206.
A rapid, dose-dependent, and significant rise in portal vein plasma GIP was found in response to increasing duodenal glucose loads, which could be described by Michaelis-Menten kinetics. Paper-3849437.
A similar ranking of plasma glucose levels occurred in the steady state, with means of 113 +/- 7 (EA), 126 +/- 3 (PA), and 184 +/- 9 (PA plus GIP) mg/dl ( P less than 0.001 by ANOVA). Paper-4871151.
The objective of this study was to determine whether bombesin- or gastrin-releasing peptide-induced release of insulin occurs before or after the release of gastric inhibitory polypeptide ( GIP) in rats. Paper-5399496.
Post-prandial plasma triglycerides, light scattering indices (LSI; an index of post-prandial chylomicronaemia) and paracetamol levels paralleled the integrated GIP responses on both normal and low-fat diets. Paper-5916235.
In conclusion, lack of GIP amplification of the late-phase plasma insulin response to glucose seems to be a consequence of diabetes mellitus, characterizing most, if not all, forms of diabetes. Paper-10031745.
Xanthan gum also tended to lower fasting and postload levels of gastrin and gastric inhibitory polypeptide ( GIP) and fasting levels of total and VLDL triglyceride and cholesterol in VLDL and LDL fractions. Paper-4937049.
These results might be compatible with the hypothesis that in obesity, hyperinsulinemia, and overactivity of the GIP cells are associated phenomena caused by overeating and reversed by reduced food intake. Paper-3697186.
Nimodipine also inhibited the potentiation of glucose-stimulated insulin secretion by GIP and GLP-I without inhibition of the stimulatory effect of these two peptides on cAMP accumulation. Paper-7639767.
The effect of beta-adrenergic receptor stimulation with isoproterenol and blockade with propranolol on the release of gastric inhibitory polypeptide ( GIP) and insulin was investigated in seven healthy volunteers. Paper-4200096.
In addition, we examined the effect of amylin on GIP-induced insulin release in pancreata from rats pretreated with pertussis toxin, an agent which inactivates certain Gi proteins coupled to adenylate cyclase. Paper-8214427.
In summary, we describe a patient with a GIP-expressive cortisol and androgen oversecreting adrenocortical nodule with the unusual presentation of hirsutism and not the typical clinical signs of Cushing's syndrome. Paper-8676525.
A chimeric promoter-reporter gene construct linking the 5'-flanking region of the hGIP gene with the thymidine kinase gene of the herpes simplex virus was introduced into the genomes of mice by microinjection. Paper-8326693.
Direct metabolic effects of gastric inhibitory polypeptide ( GIP): dissociation at physiological levels of effects on insulin-stimulated fatty acid and glucose incorporation in rat adipose tissue. Paper-5169237.
The putative proximal promoter region (800 bp) and the first exon and intron of the hGIPR gene were sequenced on adrenal DNA from nine GIP-dependent CS, as well as on leukocyte DNA of nine normal controls. Paper-10474783.
These results indicate that the GIP deficiency caused by removal of the jejunum may play a role in the poor insulin response to luminal stimuli, which contributes to glucose intolerance. Paper-6264715.
GIP stimulated adenosine 3', 5'-cyclic monophosphate ( cAMP) production in LGIPR2 cells, which was first detected after 1 h of stimulation, reached maximum level at 4 h, and returned to basal concentrations by 16 h. Paper-713831.
Since elevated glucose and insulin levels are found in hyperthyroidism, we compared the GIP responses to oral glucose ingestion in 12 hyperthyroid patients and 10 age-matched controls. Paper-4849000.
I propose that, in subjects expressing T54, the secretion of gastric inhibitory polypeptide ( GIP) evoked by fatty meals is subnormal, such that adipocytes are less efficient in converting chylomicrons to stored triglyceride. Paper-9987387.
We report on a screening of 23 surgically removed, cortisol-secreting ATs for the expression of receptors for luteinizing hormone (LH), gastric-inhibitory polypeptide ( GIP), and vasopressin (V(1a), V(1b), and V(2)). Paper-15188620.
The effect of duodenal acidification on the glucose-stimulated GIP and insulin release was investigated in man by intraduodenal infusion of glucose with a pH of 6.5 of 1.5 (no. = 7). Paper-3708433.
Porcine gastric inhibitory polypeptide ( GIP) was infused iv (120 micrograms in 60 min) in seven patients with biopsy-proven hepatic cirrhosis who had surgical porta-caval anastomoses and hyperglucagonemia in the postabsorptive state. Paper-6865271.
Culturing rat and human pancreatic islets in >or=11 mM glucose for up to 24 h resulted in prevention of GIP-mediated intracellular cAMP increase compared with culturing in 5 mM glucose. Paper-13364610.
Neither GIP nor its effects have been described in the central nervous system, and mRNA for the known peptide ligand for the receptor cannot be detected in the brain by in situ hybridization or polymerase chain reaction. Paper-7631130.
We conclude that normal aging is characterized by a decreased beta-cell sensitivity to GIP during modest hyperglycemia, which may explain, in part, the age-related impairment in glucose-induced insulin release. Paper-1529503.
6. The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine. Paper-6129802.
The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP. Paper-3969283.
In conclusion, the present study indicates that the role of the vagus nerve on GIP secretion is tiny, if any, and that the nervous influence does not overcome the effect of intraluminal administration of glucose. Paper-4854539.
To investigate specific signaling components that may mediate the effects of GIP, we analyzed Akt, glucose transporter-4, and glucose uptake, all of which are modulated by insulin in fat cells. Paper-12630473.
In the clonal pancreatic beta cell line BRIN-BD11, (Pro(3))GIP over the concentration range 10(-13) to 10(-8) M dose dependently inhibited GIP-stimulated (10(-7) M) insulin release (1.2- to 1.7-fold; P < 0.05 to P < 0.001). Paper-9365245.
Insulin release in vitro by isolated islets was greater during a 45-min incubation period with leucine (5-20 mM) or arginine (20 mM) plus GIP (10 ng to 10 micrograms/ml) than with either amino acid alone. Paper-4521241.
The exact understanding of GIP receptor regulation and signal transduction will aid in the understanding of the incretin hormone's failure to exert its biological action at the pancreatic B-cell in type II diabetes mellitus. Paper-385856.
Methods: The present study has examined in vitro and in vivo metabolic actions of a low molecular weight GIP receptor modulator 4-hydroxybenzoic acid 2-bromobenzylidene hydrazide (4H2BH), suitable for oral administration. Paper-16030084.
Finally, we have shown that GIP regulation of the ERK1/2 module is via Rap1 but does not involve Gbetagamma subunits nor Src tyrosine kinase, and we propose that cAMP-based regulation occurs via B-Raf in both CHO-K1 and beta-cells. Paper-9171512.
In a crossover design, subjects were given 2 g/kg body weight of sucrose or invert sugar, and responses of insulin, glucose, fructose and gastric inhibitory polypeptide ( GIP) were determined. Paper-4522002.
Changes in GIP concentrations mirrored reported changes in the hypertrophy and atrophy of the intestine in ruminants while GLP concentrations may be more dependent on the neural and endocrine factors associated with lactation. Paper-1538345.
Additional infusion of sulfated cholecystokinin-8 (25 pmol/kg.h) or the amino acid phenylalanine (1.7 mumol/kg.min) did not further stimulate insulin secretion and had no influence on the pharmacokinetics of exogenous GIP. Paper-6228803.
However, cultures taken from all four ACTH-dependent and the one food-dependent hyperplastic adrenals studied were also responsive to GIP (EC50 for cAMP, 1.3 x 10(-9) M in Cushing's disease and 4.1 x 10(-10) M in food-dependent disease). Paper-11124257.
On the other hand, infusion of naloxone 10(-6) M attenuates the inhibitory effect of N/OFQ 10(-6) M significantly (-21+/-6%; p<0.05 vs. GIP and N/OFQ).Thus, N/OFQ is an inhibitor of gastric somatostatin secretion. Paper-9302835.
This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin ( endoplasmic reticulum stress) and etoposide ( genotoxic stress). Paper-14067494.
Stimulation ofcortisol secretion by food intake has been implicated in the pathogenesis of some cases of ACTH-independent Cushing's syndrome, via an aberrant response of the adrenal glands to gastric inhibitory polypeptide ( GIP). Paper-8300077.
In order to evaluate the mechanism behind the augmented postprandial gastric inhibitory polypeptide ( GIP) release seen in patients with achlorhydria and hypergastrinemia, 8 healthy subjects were given a liquid test meal on three different days. Paper-4082300.
Patients with ulcerative colitis had significantly elevated fasting human pancreatic polypeptide (HPP) concentrations, and both basal and postprandial levels of gastrin, gastric inhibitory polypeptide ( GIP), and motilin were greater than normal. Paper-4257880.
Degradation, cyclic adenosine monophosphate production, insulin secretion, and glycemic effects of two novel N-terminal Ala2-substituted analogs of glucose-dependent insulinotropic polypeptide with preserved biological activity in vivo. Paper-9728459.
The GIP concentration in plasma increased from 36.7 (27.5-62.2) to 134 (78.9-215) pM after infusion of glucose with a pH of 6.5 and from 44.6 (23.4-60.5) to 141 (74.0-246) pM after pH 1.5 glucose. Paper-3708433.
The monoclonal antibody, when used to stain pancreatic tissue, gave negative results whereas a distinct population of gut endocrine cells was readily demonstrable, suggesting that GIP is not a constituent of the mammalian pancreas. Paper-4169856.
Therefore, 2 novel N-terminal Ala(2)-substituted analogs of GIP, with Ala substituted by 2-aminobutyric acid (Abu) or sarcosine (Sar), were synthesized and tested for metabolic stability and biological activity both in vitro and in vivo. Paper-9728459.
Therefore, this study examined the plasma stability, biological activity and antidiabetic potential of two novel NH2-terminal Ala2-substituted analogues of GIP, containing glycine (Gly) or serine ( Ser). Paper-9707514.
Prolonged saturated fat-induced, glucose-dependent insulinotropic polypeptide elevation is associated with adipokine imbalance and liver injury in nonalcoholic steatohepatitis: dysregulated enteroadipocyte axis as a novel feature of fatty liver. Paper-13578622.
To determine whether the autonomic nervous system has a direct effect on GIP secretion, six normal subjects received a 4-hr intraduodenal perfusion of glucose (225 mg/min) and polyethylene glycol on four successive days. Paper-5184771.
We conclude that abnormal expression of the GIP receptor allows adrenocortical cells to respond to food intake with an increase in cAMP that may participate in the stimulation of both cortisol secretion and proliferation of the tumor cells. Paper-1571275.
Moreover, a moderate but distinct GIP immunoreactivity was observed in the cerebral cortex, amygdala, substantia nigra, and lateral septal nucleus as well as in several nuclei in the thalamus, hypothalamus, and brainstem. Paper-13339322.
The area under the curve ( AUC) for glucose was significantly lower after administration of either analogue compared with glucose administered alone or in combination with native GIP (1.5-fold; P <0.05). Paper-9571043.
CONCLUSIONS: A trypsin/chymotrypsin inhibitor, POT II, can delay the rate of gastric emptying, and decrease postprandial plasma glucose levels, GIP levels, and serum insulin levels in type II diabetic patients diagnosed recently. Paper-8066568.
The granulocyte inhibitory protein ( GIP), a 23-kDa protein found to be significantly overexpressed in patients with chronic renal failure, increases autocrine transcription and expression of interleukin (IL) 6 and IL-8 in human mesangial cells. Paper-7922230.
Jejunal biopsies and the postprandial response of pancreatic polypeptide ( PP), gastrin, gastric inhibitory polypeptide ( GIP), and somatostatin have been examined in nine patients with celiac disease before and 1 year after gluten withdrawal. Paper-4439274.
GIP administration (20 pmol/kg BW) led to a significant rise of insulin and C-peptide concentrations in the first-degree relatives and control subjects ( P <.0001), but there was difference between groups ( P =.64 and P =.87, respectively). Paper-10073589.
However, oral msnnose or oral fructose caused no significant GIP release, yet the IRI response to a subsequent iv glucose load was moderately augmented after oral mannose or oral fructose when compared to iv glucose alone. Paper-3205496.
The sucrose-related increments in glucose, insulin, C-peptide, and gastric inhibitory polypeptide ( GIP) and the suppression of glucagon were only marginally affected by acarbose administration. Paper-490552.
Cyclic somatostatin-14 was used at physiological ( S1 : 50 pg/ml, S2 : 200 pg/ml) and supraphysiological (S3 : 666 pg/ml) concentrations whereas insulin and GIP were used at postprandial levels (100 microU/ml and 2 ng/ml respectively). Paper-5809104.
At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. Paper-385856.
In the perfused pancreas both SS-14 (6.1 x 10(-9) mol/l) and SMS (9.4 x 10(-9) mol/l) inhibited the GIP (2 x 10(-9) mol/l) or acetylcholine (1 x 10(-6) mol/l), but not 17.8 x 10(-9) mol/l glucose-stimulated insulin secretion. Paper-7583414.
When transfected stably into fibroblast CHL-cells a high affinity receptor was expressed which coupled to the adenylate cyclase with normal basal cAMP and increasing intracellular cAMP levels under stimulation with human GIP-1-42 (EC50 = 1.29 x 10(-13) M). Paper-385856.
After the R meal postprandial plasma concentrations of glucose, lactate, insulin, gastric inhibitory polypeptide ( GIP), glucagon-like peptide-1, and epinephrine were significantly lower compared with after the S meal. Paper-132887.
After glucose perfusion, maximal serum GIP concentrations for the four groups were: duodenum, 1383 +/- 152 pg per ml; proximal jejunum, 904 +/- 87 pg per ml; midjejunum, 545 +/- 91 pg per ml, and ileum 305 +/- 38 pg per ml. Paper-2892613.
In the present study, to elucidate the possible role of the autonomic nervous system in incretin effect, the effects of atropine, propranolol, metoprolol, and phentolamine on GIP- or GLP-1-induced insulin release were investigated in the rat. Paper-87784.
The mean fasting portal vein plasma GIP concentrations in the three groups were 45.0 +/- 5.0, 41.9 +/- 3.9, and 39.6 +/- 2.7 pmol/l, respectively, with the Iodo-gen tracers and 80.3 +/- 4.6, 78.4 +/- 5.4, and 85.7 +/- 3.7 pmol/l with the chloramine-T tracers. Paper-4089915.
Glucose-dependent insulinotropic polypeptide-mediated up-regulation of beta-cell antiapoptotic Bcl-2 gene expression is coordinated by cyclic AMP (cAMP) response element binding protein (CREB) and cAMP-responsive CREB coactivator 2. Paper-12742665.
Insulin, enteroglucagon, neurotensin, gastric inhibitory polypeptide ( GIP), and motilin have been measured in plasma during an oral glucose test in 76 patients before or after different upper gastrointestinal operations for peptic ulceration. Paper-4257666.
We conclude: (1) the inhibitory effect of acid secretion following ID glucose is mediated in part by the release of endogenous GIP; (2) glucose and mannitol probably inhibit gastric acid secretion by different mechanisms. Paper-2967022.
After treatment with AO-128 (0.6 mg/day) for 1 week, increases in plasma glucose and insulin levels were attenuated and the increase in plasma GIP levels was diminished, while the increase in tGLP-1 levels was sustained much longer. Paper-59336.
Alpha-adrenergic stimulation ( epinephrine + propranolol) significantly reduced the GIP response ( P less than 0.02) and completely inhibited the insulin response ( P less than 0.005) to oral glucose, compared with control experiments. Paper-3985345.
GIP stimulates insulin secretion from the pancreatic beta-cell via its G protein-coupled receptor activation of adenylyl cyclase and other signal transduction pathways, but there is little known regarding subsequent protein kinase pathways that are activated. Paper-9171512.
Antidiabetic therapy based on GIP holds great promise because of the fact that its insulinotropic action is highly dependent on the level of glucose, overcoming the sideeffects of hypoglycemia associated with the current therapy of Type 2 diabetes. Paper-13197155.
Functional studies have shown that GIP promoter reporters carrying derived alleles of these three SNPs ( haplotype GIP(-1920A)) have significantly lower transcriptional activities than those with ancestral alleles at corresponding positions ( haplotype GIP(-1920G)). Paper-15709560.
These include vasoactive intestinal polypeptide ( VIP), gastric inhibitory polypeptide ( GIP), motilin, pancreatic polypeptide ( PP), substance P, neurotensin, somatostatin, enkephalins, and a bombesin-like gastrin-releasing peptide. Paper-5850173.
The inverse relationship between insulin resistance and the insulin secretory response to glucose or GIP suggests that beta cell secretory function in response to different stimuli increases adaptively when insulin sensitivity is diminished. Paper-11074954.
To test the hypothesis that dietary fats may influence carbohydrate metabolism, serum glucose, insulin, and gastric inhibitory polypeptide ( GIP) responses to three mixed test meals of varying fatty acid composition were assessed in 12 normal subjects. Paper-5526013.
OGTT-derived indexes of glucose homeostasis were calculated; circulating lipoproteins, total antioxidant status, GIP, adiponectin, resistin, and cytokeratin-18 fragments (markers of hepatocyte apoptosis) after a high-fat meal were assessed. Paper-13578622.
The concentration of insulin in serum increased from 7 (4-12) to 34 (13-76) mU/l. During infusion with isoproterenol, plasma GIP increased from 29.9 (25.7-39.1) to 47.1 (37.2-83.8) pM and insulin from 9 (5-15) to 37 (16-72) mU/l before oral glucose. Paper-4200096.
In order to elucidate the role of the vagus nerve in the release of gastric inhibitory polypeptide ( GIP), mongrel dogs were given a 4-min intraduodenal infusion of 10 g glucose or 5 g soybean oil before and again 1 month after truncal vagotomy (TV). Paper-4902366.
The GIP-induced (2 or 20 micrograms) insulin release was partly inhibited by propranolol pretreatment (0.5 mg/kg subcutaneously [SC]), and GLP-1-induced (2 or 20 micrograms) insulin release was partly inhibited by propranolol or metoprolol (35 mg/kg SC). Paper-87784.
In the insulin-secreting beta cell line Rin m 5F, galanin, a newly discovered ubiquitous neuropeptide, inhibited, by 50%, the stimulation of insulin release induced by gastric inhibitory polypeptide ( GIP) or forskolin, i.e. two cAMP-generating effectors. Paper-6086732.
In the present study, we describe a novel case of a GIP receptor-expressive adrenocortical adenomatous nodule, detected incidentally by computed tomography scanning in a 41-yr-old lady with hirsutism but no clinical signs of Cushing's syndrome, on physical examination. Paper-8676525.
This paper describes the association among the peripheral concentrations of GIP, insulin and glucose during 50-g oral glucose tolerance tests ( OGTT) in healthy volunteers and in patients with gastrointestinal disorders, obesity, and uremia. Paper-3450797.
Similarly, integrated incremental responses of total GIP were reduced by vildagliptin by 26 and 21%, with and without glibenclamide, respectively ( vildagliptin: P = 0.017; glibenclamide: P = 0.44; interaction: P = 0.69). Paper-12598506.
In contrast to normal subjects and patients with the metabolic syndrome, patients with adrenal incidentalomas had significantly higher mean cortisol values after oral glucose intake as compared to i.v. glucose administration or GIP infusion. Paper-8399685.
METHODS: Effects of GIP and GIPR on differentiated 3T3-L1 cells were analyzed using Western blot analysis, Oil-Red-O staining, cyclic adenosine monophosphate radioimmunoassay, immunofluorescence microscopy, and glucose uptake measurements. Paper-12630473.
The effect of intravenous glucagon infusion on serum levels of immunoreactive GIP (IR- GIP), insulin ( IRI), gastrin (IRG), and on blood glucose has been investigated in six healthy volunteers in the fasting state and during ingestion of a mixed standard meal. Paper-2695766.
Serum GIP, insulin, and glucose concentrations were determined during a standard oral glucose tolerance test in 80 individuals, 45 of whom were normal and 35 of whom had adult-onset diabetes mellitus according to USPHS criteria. Paper-2507187.
During intraduodenal infusion of glucose, insulin concentrations in plasma were also decreased by morphine, an effect best explained by decreased small intestinal transit with delayed absorption of glucose and delayed release of GIP. Paper-5167492.
Multiple logistic regression analysis showed that the highest quartile of fasting GIP levels was associated with a significantly high risk of colorectal adenoma ( odds ratio, 2.1; 95% confidence interval, 1.08-3.96; P = .01) in comparison with the lowest quartile. Paper-16151215.
It has recently been suggested that gastric inhibitory polypeptide ( GIP) may block the risk factors associated with both hypo- and hyperglycemia by either suppressing or enhancing (depending on the prevailing glucose conditions) insulin release. Paper-8064245.
The diurnal variations of serum gastric inhibitory polypeptide ( GIP), serum insulin, plasma glucagon, plasma glucose and serum triglycerides were studied for 24 hr in 6 healthy young men, consuming three meals and performing their usual physical activities. Paper-4517100.
GIP potentiated glucose-induced beta-(INS-1)-cell growth to levels comparable with GH and GLP-1 while promoting cell survival in the face of serum and glucose-deprivation or treatment with wortmannin or streptozotocin. Paper-10004097.
In macronodular adrenal hyperplasia, we have identified, in addition to GIP-dependent Cushing's syndrome, other patients in whom cortisol production was regulated abnormally by vasopressin, ss-adrenergic receptor agonists, hCG/LH, or serotonin 5HT-4 receptor agonists. Paper-8626723.
When injected subcutaneously in normal Wistar, Fa/?, or fa/fa Vancouver Diabetic Fatty (VDF) Zucker rats, both GIP and [D-Ala(2)]GIP significantly reduced glycemic excursions during a concurrent oral glucose tolerance test via stimulation of insulin release. Paper-9391745.
CONCLUSIONS: In conclusion, GIP in combination with hyperinsulinemia and slight hyperglycemia increased adipose tissue blood flow, glucose uptake, and FFA re-esterification, thus resulting in increased TAG deposition in abdominal subcutaneous adipose tissue. Paper-15380954.
Plasma concentrations of gastric inhibitory polypeptide ( GIP) were measured in preruminant goat kids before and after consumption of milk, skimmed milk or solutions of milk fat, lactose, glucose or casein plus lactose. Paper-7607641.
The presence of insulin + GIP in the incubation medium stimulated glucose incorporation into hepatic total lipids in the maize-oil ( P < 0.01) and fish-oil groups ( P < 0.05), as well as into hepatic triacylglycerol in the maize-oil group ( P < 0.005). Paper-381482.
Blood glucose, gastric inhibitory polypeptide ( GIP), vasoactive intestinal polypeptide (VIP) and gastrin secretions were measured over a three-hour period following the ingestion by normal subjects of a mixed meal with two different caloric levels (1055 Kcal and 1192 Kcal). Paper-4567650.
This review attempts to provide a comprehensive picture of the role of GIP in the central nervous system and to highlight recent findings from our group showing its potential involvement in neurological illnesses including epilepsies, Parkinson's disease and Alzheimer's disease. Paper-15367591.
The plasma concentrations of gastrin, gastric inhibitory polypeptide ( GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide ( PP) were studied following the ingestion of a protein rich meal in late pregnancy and postpartum in 11 normal women. Paper-3938795.
Increased mucosal concentrations of all peptides except vasoactive intestinal polypeptide ( VIP) were found in coeliac disease and selective increases of VIP found in Crohn's disease, motilin in the irritable bowel syndrome and gastrin and GIP in pancreatic insufficiency. Paper-4725238.
Analysis of biochemical parameters among the three genotypes showed a significant association of total cholesterol ( P = 0.042) and low density lipoprotein (LDL) with the G allele of the SNP rs2291726 in GIP ( P = 0.004), but this was observed only in the case of female subjects. Paper-15361815.
Taken together, these studies show that GIP and insulin act in a synergistic manner on 3T3-L1 cell development and that adipocyte GIPR expression is upregulated through a mechanism involving interactions between PPARγ and a GIPR promoter region containing an acetylated histone region. Paper-15761807.
The effect of a dialysate exchange with both 1.5 and 4.25% glucose solutions on plasma levels of glucose, insulin, gastric inhibitory polypeptide ( GIP), and glucagon has been investigated in 5 continuous ambulatory peritoneal dialysis ( CAPD) patients. Paper-4834251.
The effect of aging, obesity, and non-insulin-dependent diabetes mellitus on glucose-stimulated gastric inhibitory polypeptide ( GIP) levels was studied in 55 male subjects, ranging in age from 19 to 84 yr, and in obesity, expressed as body mass index, from 21 to 34. Paper-4547865.
RESULTS: Serum insulin, plasma glucose, plasma gastric inhibitory polypeptide ( GIP) values, and the rate of gastric emptying were all significantly ( P < 0.05) decreased over the 2-h testing period when POT II was added to the oral glucose/protein meal. Paper-8066568.
SMS (9.4 x 10(-8) mol/l) also inhibited somatostatin release stimulated by gastric inhibitory polypeptide ( GIP), but did not suppress gastrin release under the same conditions; an opposite effect was obtained when l-isoproterenol was used to stimulate somatostatin release. Paper-7583414.
These findings suggest that, at term gestation, the newborn infants have a "functional" enteroinsular axis in response to glucose, i.e. the rising plasma GIP contributed in part to the enhanced insulin response to enterally infused glucose.(ABSTRACT TRUNCATED AT 250 WORDS) Paper-6443325.
The interaction of three incretin candidates, glucagon-like peptide-1(7-36)amide (t-GLP-1), gastric inhibitory polypeptide ( GIP), and sulfated COOH-terminal octapeptide of cholecystokinin (CCK-8-S), on insulin and glucagon release from the isolated perfused rat pancreas was studied. Paper-56633.
Transfection of chimeric chloramphenicol acetyltransferase plasmids containing various deletions of the human gastric inhibitory polypeptide ( GIP) promoter into hamster insulinoma (HIT T15) cells indicated that the region between -180 and +14 is sufficient for basal promoter activity. Paper-7571970.
With single infusions of GIP or GLP-1 (circulating concentrations, 464 +/- 73 and 54 +/- 3 pmol/L, respectively), B-cell responses were significantly augmented compared to i.v. glucose alone and were no longer significantly different from those after oral glucose. Paper-88137.
On the other hand, plasma levels of insulin greatly increased immediately after glucose ingestion in accordance with a rapid elevation of plasma GIP in 11 gastrectomized patients in whom the duodenum and the pancreas were preserved intact and who served as the control group. Paper-4818313.
Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Paper-2475637.
In conclusion, prostaglandin E analogues which caused a reduction in GIP responses, and thereby disrupting the enteroinsular axis to varying degrees, delayed the time-course of insulin secretion without a significant impact on glucose tolerance.(ABSTRACT TRUNCATED AT 250 WORDS) Paper-6179692.
With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. Paper-9054361.
To determine the site of endogenous release of gastric inhibitory polypeptide ( GIP), glucose perfusions (556 mmoles per liter) of duodenum, proximal jejunum, midjejunum, and ileum were performed in human volunteers using an occluding balloon perfusion technique. Paper-2892613.
In the present investigation, the gastrin, gastric inhibitory polypeptide ( GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, pancreatic glucagon, and pancreatic polypeptide ( PP) responses to a protein rich meal in pregnancy and postpartum were studied in 10 women with gestational diabetes. Paper-4163977.
In contrast, GIP enhanced basal corticosterone secretion and cyclic-AMP release by dispersed inner adrenocortical cells in a concentration-dependent manner, and the maximal effective concentration (10(-7) M) evoked 1.5- and 2.4-fold rises in corticosterone and cyclic-AMP production, respectively. Paper-8307973.
There were significant positive correlations between postmeal splanchnic glucose output and both IRI ( r = 0.805, P less than 0.005) and GIP ( r = 0.749, P less than 0.02) in the diabetic patients but not in the normal subjects ( r = 0.10, P = NS for both). Paper-5165661.
The results suggest that structural integrity of the glucose molecule from the C-1 to C-4 carbon atoms, a free aldehyde group on the C-1 carbon atom, and a cyclic structure are all necessary for both the active transport of glucose and the release of endogenous GIP. Paper-4318383.
Enprostil almost totally inhibited the GIP response (by 94%; P less than or equal to 0.001), delayed initial insulin and C-peptide responses, but reduced the integrated incremental C-peptide response (which corresponds to the overall release of insulin) by only 14% ( P less than or equal to 0.05). Paper-6179692.
In diseases with associated mucosal inflammation (coeliac disease, Crohn's disease with jejunal involvement, postinfective tropical malabsorption, and common variable immunodeficiency) there was a selective increase in fragility of the gastric inhibitory polypeptide ( GIP) and somatostatin storage granules. Paper-4725238.
The mean levels of fasting GIP (34.9 ± 49.5 vs 25.0 ± 20.1 pg/mL, P = .04), triglyceride, glucose, and insulin and the values of the homeostasis model assessment of insulin resistance in the colorectal adenoma group were significantly higher than those in the control group. Paper-16151215.
We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. Paper-14067494.
Interestingly, both exendin-4 and exendin-(9-39) were antagonists of the receptor, inhibiting GIP-induced cAMP formation by up to 60% when present at a concentration of 10 mumol/l. Finally, the physical and genetic chromosomal localization of the receptor gene was determined to be on 19q13.3, close to the ApoC2 gene. Paper-357812.
However exendin-4 and exendin-(9-39) at 1 mumol/l displaced binding by approximately 70 and approximately 100% at 10 mumol/l. GIP binding to both forms of the receptor induced a dose-dependent increase in intracellular cAMP levels (EC50 values of 0.6-0.8 nmol/l) but no elevation of cytoplasmic calcium concentrations. Paper-357812.
Circulating enteroglucagon and GIP concentrations at the age of 2 h were significantly higher than those observed in cord blood in both the IDM and the control infants, but the IDM had significantly lower blood glucose levels, higher plasma C-peptide, and lower enteroglucagon concentrations before the first feed. Paper-7844046.
Since pancreatic insulin secretion (C-peptide), glucagon secretion, and the entero-insulinar axis ( GIP) are not impaired in these non-cirrhotic patients with idiopathic haemochromatosis, iron accumulation in the hepatocytes may be responsible for the impaired insulin effect and may cause impaired hepatic insulin extraction. Paper-4546361.
Serum levels of glucose, insulin, and gastric inhibitory polypeptide ( GIP) in response to intraduodenal and intravenous glucose loads have been examined in rats with exocrine pancreatic atrophy induced by feeding them a copper-deficient diet supplemented with D-penicillamine for 10-12 weeks. Paper-5849927.
Three months after surgery, fasting plasma ACTH and cortisol were suppressed, but cortisol increased 3.6-fold after oral glucose, whereas ACTH remained suppressed; this was inhibited by octreotide pretreatment, suggesting that cortisol secretion by the left adrenal is also GIP dependent. Paper-1942296.
To obtain molecular evidence for the vagal chemoreception of GLP-1, the concept derived from those electrophysiological observations, receptor gene expressions of GLP-1 and GIP in the rat nodose ganglion were examined by means of reverse transcriptase-mediated polymerase chain reaction ( RT-PCR) and Northern blot analysis. Paper-10406513.
Transient overexpression in INS-1 beta-cells (clone 832/13) of wild-type (WT) K(V)1.4, or a T601A mutant form resistant to PKA phosphorylation, resulted in reduced glucose-stimulated insulin secretion; WT K(V)1.4 overexpression potentiated GIP-induced insulin secretion, whereas this response was absent in T601A cells. Paper-10784581.
Moreover, multivariate linear regression analysis showed that the presence of acromegalic status was associated with higher fasting and postprandial GIP levels independently of sex, age, fasting and postprandial plasma glucose and insulin levels, and the occurrence of normal or impaired glucose tolerance. Paper-8994316.
Changes in blood flow in the celiac artery, superior mesenteric artery, and pancreas in response to an intravenous injection of synthetic human gastric inhibitory polypeptide ( GIP) were determined simultaneously and continuously in anesthetized dogs, using a transit-time ultrasonic flowmeter and a laser-Doppler flowmeter. Paper-5848802.
The plasma gastric inhibitory polypeptide ( GIP), pancreatic glucagon-like immunoreactivity (PGLI), and gut glucagon-like immunoreactivity (GGLI) responses to oral glucose have been measured in five patients with chronic pancreatitis (with diabetic glucose tolerance tests) and in matched nondiabetic controls. Paper-2475637.
We have investigated the pancreatic alpha and beta cell function by measuring insulin ( IRI), C-peptide ( CPR), glucagon (IRG), somatostatin (SLI), and gastric inhibitory polypeptide ( GIP) in amniotic fluid collected during basal conditions or 2 h after an arginine test in 92 diabetic and 32 non-diabetic pregnant women. Paper-5383674.
Under metabolic ward conditions oral glucose tolerance test was performed before and after the training period with the same energy intake quantitatively and qualitatively, and glucose, insulin, connecting (C)-peptide, gastric inhibitory polypeptide ( GIP) and pancreatic polypeptide ( PP) were determined. Paper-4544950.
Expressing glucose disposal as glucose metabolic clearance rate demonstrated that elevated, but still physiological GIP levels had no effect on NIMGU but significantly increased insulin-mediated glucose uptake when plasma insulin levels were similar to levels typically observed after a meal. Paper-1698880.
Misoprostol and rioprostil reduced integrated incremental responses of GIP by 57% ( P less than or equal to 0.001) and 45% ( P less than or equal to 0.01), respectively, and both gave rise to an initial (approximately 10 min) delay of insulin and C-peptide responses, without a significant overall reduction in integrated incremental responses. Paper-6179692.
Postprandial TAG, non-esterified fatty acids (NEFA), ketones, glucose, insulin and gastric inhibitory polypeptide ( GIP) responses were monitored in sixteen normal adult male subjects over 6 h following consumption of test meals containing dietary TAG in which palmitic acid was predominantly on the sn-1 (Control) or sn-2 positions (Betapol). Paper-8091728.
The combination of PN with EN resulted in lower interstitial glucose concentrations (P = 0.002), reduced insulin resistance, improved insulin sensitivity (HOMA-insulin resistance (IR) P = 0.045; HOMA beta P = 0.037; ITT P = 0.006), improved intestinal permeability (P < 0.001) and increased GIP (P = 0.01) when compared with PN alone. Paper-15143402.
Blunting the insulin response to glucose directly by delaying glucose absorption and indirectly through reducing GIP secretion, may be a valuable therapeutic approach in reactive hypoglycemia; nevertheless, long-term study with Miglitol are needed, due to the poor intestinal tolerance of this drug in the present acute study. Paper-6897437.
We have performed oral glucose tolerance tests ( OGTT) in nine patients with prolactinomas, eight patients with active acromegaly, five patients with acromegaly in remission and nine normal controls, and measured blood glucose, plasma insulin, pancreatic glucagon, enteroglucagon, gastric inhibitory polypeptide ( GIP) and GH during the test. Paper-4517340.
RESULTS: During GIP and HI-HG clamp, abdominal subcutaneous adipose tissue blood flow, hydrolysis of circulating triacylglycerol (TAG) ( P = 0.009), and glucose uptake ( P = 0.03) increased significantly while free fatty acid (FFA) output ( P = 0.04) and FFA/ glycerol release ratio ( P = 0.02) decreased compared with saline and HI-HG clamp. Paper-15380954.
Perfusates containing glucose, sucrose, galactose, maltose, 3-O-methylglucose or alpha- or beta- methylglucoside at concentrations of 100 mmol/l in Krebs-Ringer phosphate buffer (KRP) produced significant stimulation of GIP release compared with the control perfusions with KRP alone ( P less than 0.02). Paper-3580374.
These synonyms are used for gene GIP (gastric inhibitory polypeptide): Glucose-dependent insulinotropic polypeptide, Gastric inhibitory polypeptide.
These accession numbers are used for gene GIP: Q6NTD3 (UNIPROT__AC), Q4VB42 (UNIPROT__AC), HQ448468 (NCBI_GENBANK__AC), BC069100 (NCBI_GENBANK__AC).
GIP is a homologue of GIP (gastric inhibitory polypeptide) from Pan troglodytes.
GIP is a homologue of GIP (gastric inhibitory polypeptide) from Canis lupus familiaris.
GIP is a homologue of GIP (gastric inhibitory polypeptide) from Bos taurus.
GIP is a homologue of Gip (gastric inhibitory polypeptide) from Mus musculus.
GIP is a homologue of Gip (gastric inhibitory polypeptide) from Rattus norvegicus.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.