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Lipotransin: a novel docking protein for hormone-sensitive lipase. Paper-1951193.
HSL activity was also suppressed by TNF-alpha. Paper-15338608.
In the absence of TNF-alpha, Met enhanced the HSL activity. Paper-15338608.
Mice lacking both Nceh1 and Lipe aggravated atherosclerosis in an additive manner. Paper-13968008.
Functional interaction of hormone-sensitive lipase and perilipin in lipolysis. Paper-14120421.
In these studies, we provide direct evidence for a physical interaction of HSL with Plin. Paper-14120421.
Vimentin is a functional partner of hormone sensitive lipase and facilitates lipolysis. Paper-14695726.
In the presence of TNF-alpha, Met, Cys and CysH suppressed the HSL activity. Paper-15338608.
Thus, HSL translocation requires the phosphorylation of both HSL and perilipin. Paper-10162803.
Thus, PKA-induced HSL translocation was independent of perilipin phosphorylation. Paper-12027736.
There is evidence of both HSL and ATGL activity and/or expression in skeletal muscle. Paper-12757783.
HSL and ATGL mRNA levels increased concomitantly during adipocyte differentiation. Paper-11527508.
Perilipin A is essential for the translocation of hormone-sensitive lipase during lipolytic activation. Paper-9661828.
The double-Tg mice ( MHC- HSL) were maintained with doxycycline (Dox) to suppress Tg HSL. Paper-9062051.
The deficiency of HSL also diminished the islet mass in Lep(ob/ ob) mice due to decreased cell proliferation. Paper-13930601.
Thus, ATGL and HSL coordinately catabolize stored triglycerides in adipose tissue of mammals. Paper-10898734.
These concentrations of ethanol had no effect on the activity of either LPL or HSL in vitro. Paper-993115.
Fatty acid-binding protein- hormone-sensitive lipase interaction. Fatty acid dependence on binding. Paper-10041282.
HSL expression and nCEH activity in these cells and in peritoneal macrophages were comparable. Paper-1467256.
Together, ATGL and HSL are responsible for more than 95% of the TG hydrolase activity present in murine WAT. Paper-12365744.
Perilipin (encoded by the gene Plin), an adipocyte protein, has been postulated to modulate HSL activity. Paper-8614561.
In the absence of fatty acids, no FABP- HSL association could be demonstrated for any FABP form. Paper-10041282.
Perilipin targets a novel pool of lipid droplets for lipolytic attack by hormone-sensitive lipase. Paper-11006744.
Thus, the lipolytic action(s) of HSL at the LD surface requires PKA-dependent perilipin phosphorylation. Paper-12027736.
Stimulation of lipolysis and hormone-sensitive lipase via the extracellular signal-regulated kinase pathway. Paper-8863442.
Absence of hormone-sensitive lipase inhibits obesity and adipogenesis in Lep ob/ ob mice. Paper-10238059.
Overexpression of human lipoprotein lipase increases hormone-sensitive lipase activity in adipose tissue of mice. Paper-273815.
Hormone-sensitive lipase maps to proximal chromosome 7 in mice and is genetically distinct from the Ad and Tub loci. Paper-8120857.
The action of ZAG is associated with reduced FAS expression and increased HSL expression in the liver of obese mice. Paper-15551178.
Hormone-sensitive lipase deficiency suppresses insulin secretion from pancreatic islets of Lep ob/ ob mice. Paper-13930601.
Short-term treatment with GLP-1 increased HSL activity without changing the expression of the beta-cell isoform of HSL. Paper-12373668.
We show here that targeted disruption of Plin results in healthy mice that have constitutively activated fat-cell HSL. Paper-8614561.
Inhibitory effect of tumor necrosis factor on gene expression of hormone sensitive lipase in 3T3-L1 adipocytes. Paper-6665289.
From in vitro assays, HSL is known to hydrolyze TG, diglycerides (DG), cholesteryl esters, and retinyl esters. Paper-9155774.
Plin is required for the translocation of hormone-sensitive lipase ( HSL) from the cytosol to lipid droplets upon stimulation. Paper-14120421.
Each of these proteins (Peri A, ATGL, and HSL) has been demonstrated to regulate lipid storage and release in the adipocyte. Paper-14342282.
In addition, antibody titration showed that essentially all nCEH activity in murine macrophages was accounted for by HSL. Paper-1467256.
The current studies provide evidence that vimentin participates in lipolysis through direct, hormonally regulated interactions with HSL. Paper-14695726.
These results suggested that the reduction in HSL activity caused by TNF resulted from inhibited gene expression of the enzyme. Paper-6665289.
Thus, lipotransin is a novel docking protein that may direct the hormonally regulated redistribution of hormone-sensitive lipase. Paper-1951193.
NCEH activities were completely absent from both brown adipose tissue (BAT) and white adipose tissue (WAT) in HSL-/- mice. Paper-2112926.
Lipotransin is a novel hormone-sensitive lipase (HSL)-interacting protein that appears to translocate HSL to the lipid droplet. Paper-1951193.
PSE inhibits a number of lipases, including PL, LPL and, possibly, hormone sensitive lipase ( HSL). Paper-11830207.
Thus, the responses of the residual lipolytic activity to lipolytic hormones and TNF-alpha were well conserved in the absence of HSL. Paper-9234401.
These results redefine and expand our understanding of how perilipin regulates HSL-mediated lipolysis in adipocytes. Paper-12027736.
Thus, deficiency of both leptin and HSL has unmasked novel roles of HSL in adipogenesis as well as in feeding behavior. Paper-10238059.
To compare binding to catalysis, each FABP isoform was incubated with HSL in vitro, and enzymatic activity was assessed. Paper-10041282.
These results strongly suggest that elevated B56alpha/ PP2A inhibits HSL and lipolysis in white adipose tissue of DIO mice. Paper-15318506.
Modulation of hormone-sensitive lipase and protein kinase A- mediated lipolysis by perilipin A in an adenoviral reconstituted system. Paper-9157366.
GLP-1 also rescued GSIS in HSL(-/-) mice, indicating that signaling via HSL is not a major pathway for its incretin effect. Paper-10532882.
We further demonstrate that Nceh1 and Lipe mediate a comparable degree of nCEH activity in macrophages and together account for most of the activity. Paper-13968008.
The activation by A-FABP was dependent upon its fatty acid binding properties because a non-fatty acid binding mutant, R126Q, failed to activate HSL. Paper-10041282.
Furthermore, FAS mRNA expression decreased ( P < 0.01) and HSL mRNA expression increased ( P < 0.001) in the liver in ZAG over-expressing mice. Paper-15551178.
Adipose triglyceride lipase and hormone-sensitive lipase are the major enzymes in adipose tissue triacylglycerol catabolism. Paper-12365744.
We generated mice lacking both leptin and HSL Lep(ob/ob)/HSL(-/-) and explored the role of HSL in pancreatic beta-cells in the setting of obesity. Paper-13930601.
Hormone-sensitive lipase has a role in lipid signaling for insulin secretion but is nonessential for the incretin action of glucagon-like peptide 1. Paper-10532882.
Apelin increased HSL phosphorylation at Ser-565 and also abrogated isoproterenol-induced HSL phosphorylation at Ser-563. Paper-15592118.
Dysregulation of lipolysis and lipid metabolism in visceral and subcutaneous adipocytes by high-fat diet: role of ATGL, HSL, and AMPK. Paper-14683332.
Adenoviral overexpression of HSL and/or ATGL reduced liver triglycerides by 40-60% in both ob/ob mice and mice with high fat diet-induced obesity. Paper-14315459.
Deletion of genes encoding ATGL ( Pnpla2) or HSL ( Lipe) in mice results in striking phenotypic differences, suggesting distinct roles for these lipases. Paper-12843361.
Regulation of Pnpla2, Lipe, and Mgll, which are involved in triglyceride hydrolysis, was studied under conditions of elevated hepatic lipids. Paper-13454379.
PKA-stimulated lipolysis by non- HSL additionally requires phosphorylation of one or more PKA sites within Peri 301-517 (Ser433, Ser492, and Ser517). Paper-10066745.
This reaction is mediated by hormone-sensitive lipase ( HSL), a cytosolic enzyme, and perilipin, which coats the lipid droplet surface in adipocytes. Paper-10162803.
These results demonstrate for the first time the relative contributions of ATGL, HSL, and Peri A on determination of LD size in the absence of PKA stimulation. Paper-14342282.
Fatty acid synthase and hormone-sensitive lipase expression in liver are involved in zinc-alpha2-glycoprotein-induced body fat loss in obese mice. Paper-15551178.
Perilipin promotes hormone-sensitive lipase-mediated adipocyte lipolysis via phosphorylation-dependent and -independent mechanisms. Paper-12027736.
Chromosomal localization of lipolytic enzymes in the mouse: pancreatic lipase, colipase, hormone-sensitive lipase, hepatic lipase, and carboxyl ester lipase. Paper-101357.
In summary, hepatic overexpression of HSL or ATGL can promote fatty acid oxidation, stimulate direct release of free fatty acid, and ameliorate hepatic steatosis. Paper-14315459.
ATGL and HSL are robustly expressed by adipocytes that we generated from murine embryonic fibroblasts of perilipin knock-out mice. Paper-12395121.
The effect of glucagon-like peptide 1 ( GLP-1) on GSIS was also studied, as GLP-1 could augment GSIS via protein kinase A activation of HSL and lipolysis. Paper-10532882.
The inhibitory effect of LC-CoA on adipocyte HSL was dependent on phosphorylation and enhanced by acyl-CoA-binding protein ( ACBP). Paper-11096239.
Adipose lipolysis is mediated, in part, via interaction of fatty acid-binding protein ( FABP) with hormone-sensitive lipase ( HSL). Paper-10041282.
Tumor necrosis factor increases the rate of lipolysis in primary cultures of adipocytes without altering levels of hormone-sensitive lipase. Paper-121665.
When bound to hormone sensitive lipase ( HSL), StAR shuttles free cholesterol into the mitochondria for downstream conversion into androgens. Paper-14167002.
The deficiency of HSL exacerbated the accumulation of triglycerides in Lep(ob/ ob) islets, leading to reduced glucose-stimulated insulin secretion. Paper-13930601.
Plasma 3-beta-hydroxybutyrate levels were increased 3-5 days after infection in both HSL- and ATGL-overexpressing male mice, suggesting an increase in beta-oxidation. Paper-14315459.
Induction of inflammatory markers in vivo and in vitro was preceded by phosphorylation of p38 and JNK, and inhibition of HSL prevented activation of these kinases. Paper-15215987.
We show that 76-0079 had no effect on TG catabolism in HSL-deficient WAT but, in contrast, essentially abolished free fatty acid mobilization in ATGL-deficient fat. Paper-12365744.
It is believed that perilipin phosphorylation is essential for the translocation of HSL from the cytosol to the LD, a key event in stimulated lipolysis. Paper-12027736.
Adipose triglyceride lipase ( ATGL) and hormone-sensitive lipase ( HSL) are the major rate-determining enzymes for lipolysis in adipocytes. Paper-14342282.
TGH is responsible for a major part of non- HSL lipase activity in WAT in vitro and may mediate some or all HSL-independent lipolysis in adipocytes. Paper-10612459.
This suggests that PKA-dependent perilipin phosphorylation facilitates (either direct or indirect) perilipin interaction with LD- associated HSL. Paper-12027736.
The N-terminal construct, Plin 1-200, which does not associate with lipid droplets but interacts with HSL, can function as a dominant negative for PKA-stimulated lipolysis. Paper-14120421.
Basal insulin secretion was increased, whereas GLP-1 potentiation of GSIS was decreased in islets isolated from HSL-/- mice, as compared to islets from wild type mice. Paper-12373668.
In Peri-/- MEF adipocytes, PKA activation significantly enhanced the amount of HSL that could be cross- linked to and co-immunoprecipitated with ectopic Peri A. Paper-12027736.
PKA site mutagenesis revealed that PKA-stimulated lipolysis by HSL requires phosphorylation of one or more sites within Peri 1-300 (Ser81, Ser222, and Ser276). Paper-10066745.
In this study, we utilize an adenoviral system to knockdown or overexpress ATGL and HSL in an engineered model system of adipocytes in the presence or absence of Peri A. Paper-14342282.
Together, these results demonstrate that FFAs liberated by HSL activate p38 and JNK, and p38 mediates pro-inflammatory cytokine expression in adipose tissue. Paper-15215987.
We have also reconstructed the HSL translocation reaction in the nonadipocyte Chinese hamster ovary cell line by introduction of GFP-tagged HSL with and without perilipin A. Paper-9661828.
PKA-stimulated HSL translocation was confirmed in differentiated brown adipocytes from perilipin null mice expressing an adipose-specific Peri Adelta1-6 transgene. Paper-12027736.
The mRNA levels of hormone-sensitive lipase ( HSL) and HSL activity in adipose tissue during feeding were higher in LPL transgenic mice than in controls. Paper-273815.
Hepatic overexpression of hormone-sensitive lipase and adipose triglyceride lipase promotes fatty acid oxidation, stimulates direct release of free fatty acids, and ameliorates steatosis. Paper-14315459.
The mRNA expressions of fatty acid synthase ( FAS) and hormone-sensitive lipase ( HSL) in liver tissue were determined by reverse transcription-polymerase chain reaction. Paper-15551178.
Hormone-sensitive lipase deficiency in mice changes the plasma lipid profile by affecting the tissue-specific expression pattern of lipoprotein lipase in adipose tissue and muscle. Paper-9159903.
Hepatic esterified cholesterol content and ATP-binding cassette transporter A1 ( ABCA1) mRNA and protein levels were increased in HSL-null mice regardless of the dietary regimen. Paper-13033315.
Thus, activation of the ERK pathway appears to be able to regulate adipocyte lipolysis by phosphorylating HSL on Ser(600) and increasing the activity of HSL. Paper-8863442.
We show that arachidonic acid induces androgen production in steroid starved LNCaP cells coincidently in the same conditions that HSL and StAR are predominantly localized in the mitochondria. Paper-14167002.
In conclusion, HSL is the major lipase for catecholamine- and natriuretic peptide-stimulated lipolysis, whereas ATGL mediates the hydrolysis of triglycerides during basal lipolysis. Paper-11527508.
Importantly, each FABP form stimulated HSL activity approximately 2-fold using cholesteryl oleate as substrate but exhibited no activation using p-nitrophenyl butyrate. Paper-10041282.
The interaction of the two proteins depends upon the phosphorylation of HSL by protein kinase A. Once formed, the complex is dissociated by ATP hydrolysis, due to the ATPase activity of lipotransin. Paper-1951193.
While Lipe deficiency remarkably reduced the neutral cholesterol ester hydrolase activity in adrenal glands as previously reported, additional inactivation of Nceh1 gene completely abrogated the activity. Paper-15609049.
Moreover, hormone-sensitive lipase ( HSL) protein was increased 4.3-fold in adipocytes from IRS-1-null mice compared with wild-type mice, and HSL mRNA expression was also increased. Paper-8970967.
Our results demonstrate a role for perilipin in reining in basal HSL activity and regulating lipolysis and energy balance; thus, agents that inactivate perilipin may prove useful as anti-obesity medications. Paper-8614561.
Based on the time-dependent aspects of TNF alpha stimulation and the lack of change in immunoreactive HSL, the findings suggest a TNF-induced posttranslational modification of the enzyme. Paper-121665.
It is known that upon lipolytic hormone stimulation, protein kinase A phosphorylates HSL Ser660 and activates HSL, whereas protein phosphatase 2A ( PP2A) dephosphorylates and inactivates HSL. Paper-15318506.
On activation of protein kinase A, HSL-GFP translocates to lipid droplets only in cells that express fully phosphorylatable perilipin A, confirming that perilipin is required to elicit the HSL translocation reaction. Paper-9661828.
Hormone-sensitive lipase ( HSL) is believed to play an important role in the mobilization of fatty acids from triglycerides ( TG), diglycerides, and cholesteryl esters in various tissues. Paper-9159903.
Since ANP activates guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase, HSL serine 660 is likely a substrate for cGMP-dependent protein kinase in human adipocytes. Paper-15939554.
Since HSL is expressed in islet beta-cells, this effect could contribute to the stimulation of insulin secretion by GLP-1, provided that a lipid signal of importance for insulin secretion is generated. Paper-11580815.
These results suggest that binding and activation of HSL by FABPs are separate and distinct functions and that HSL contains a site for fatty acid binding that allows for FABP association. Paper-10041282.
HSL-dependent lipolysis in response to catecholamines is mediated by protein kinase A (PKA)-dependent phosphorylation of perilipin A ( Peri A), an essential lipid droplet (LD)-associated protein. Paper-12027736.
For human subcutaneous adipocytes, isoproterenol, forskolin, and ANP activated HSL phosphorylation/colocalization, but Lys-γ3-melanocyte stimulating hormone had little or no effect. Paper-15939554.
HSL constitutes the critical enzyme in the modulation of lipid stores and the only component being subjected to hormonal control in terms of the recently identified Adipose Triglyceride Lipase ( ATGL). Paper-14470479.
Additionally, the absence of HSL in white adipose tissue caused a shift of the fatty acid composition of the TG moiety toward increased long chain fatty acids implying a substrate specificity of the enzyme in vivo. Paper-9155774.
Our data also suggested that adiponectin deficiency impair insulin action in vitro probably through the IRS-1 pathway, and increase intracellular fat accumulation partially through HSL down-regulation. Paper-14133342.
Using a tamoxifen regulatable Raf system expressed in 3T3-L1 preadipocytes, exposure to tamoxifen causes a 14-fold activation of ERK within 15-30 min and results in approximately 2-fold increase in HSL activity. Paper-8863442.
These data suggest that HSL overexpression in macrophages, alone or in combination with ACAT inhibitors, may constitute a useful therapeutic approach for impeding CE accumulation in macrophages in vivo. Paper-1467256.
The resulting HSL overexpression increased hydrolysis of cellular CEs 2- to 3-fold in lipid-laden cells in the presence of an acyl coenzyme A:cholesterol acyltransferase ( ACAT) inhibitor. Paper-1467256.
Some of these effects of sulfur amino acids were different between LPL and HSL, between the absence and the presence of TNF-alpha, and between 3T3-L1 adipocytes and the adipose tissue from rats. Paper-15338608.
It is tempting to speculate that an imbalance between ATGL and HSL expression results in incomplete lipolysis and increased accumulation of lipid intermediates in skeletal muscle of obese insulin resistant subjects. Paper-12757783.
We show that the inhibition of lipolysis through genetic ablation of adipose triglyceride lipase ( Atgl) or hormone-sensitive lipase ( Hsl) ameliorates certain features of cancer-associated cachexia (CAC). Paper-16066330.
To examine the relationship between the binding of FABP to HSL and activation of catalytic activity, isothermal titration microcalorimetry as well as kinetic analysis using a variety of FABP isoforms have been employed. Paper-10041282.
Relative protein abundance and activation of perilipin, hormone sensitive lipase ( HSL), adipose triglyceride lipase ( ATGL), and adipose differentiation related protein (ADRP) were determined by western blotting. Paper-16104869.
In this report, we show that the CE hydrolysis catalyzed by neutral cholesterol ester hydrolase ( nCEH) can be modulated by overexpression of hormone-sensitive lipase ( HSL) in macrophage foam cells. Paper-1467256.
The results suggest the translocation of HSL to the lipid droplet occurs by virtue of Plin localization to the surface of lipid droplets and a physical interaction of HSL occurring with sequences within the N-terminal region of Plin. Paper-14120421.
To explore the role of HSL in the metabolism of fat and carbohydrate, we have generated mice lacking both leptin and HSL (Lep(ob/ob)/HSL(-/-)) by cross-breeding HSL(-/-) mice with genetically obese Lep(ob/ ob) mice. Paper-10238059.
In the present study, we found that mice lacking both leptin and HSL (Lep(ob/ob)/HSL(-/-)) showed massive accumulation of CE in the liver compared with Lep(ob/ob)/HSL(+/+) mice, while triacylglycerol ( TG) accumulation was modest. Paper-12881120.
HSL is a substrate of activated ERK and site-directed mutagenesis of putative ERK consensus phosphorylation sites in HSL identified Ser(600) as the site phosphorylated by active ERK. Paper-8863442.
Our results demonstrate that HSL deficiency markedly affects the metabolism of TG-rich lipoproteins by the coordinate down-regulation of VLDL synthesis and up-regulation of LPL in muscle and white adipose tissue. Paper-9159903.
Tc-responsive element- HSL transgenic (Tg) mice were generated and crossed with myosin heavy chain (MHC)alpha-tTA Tg mice, which express the Tc-responsive transactivator (tTA) in the heart. Paper-9062051.
However, in the absence of protein kinase A (PKA) stimulation (basal state), the lipases ( ATGL and HSL) are located mainly in the cytoplasm, and their contribution to basal rates of lipolysis and influence on LD size are poorly understood. Paper-14342282.
In addition, the possible involvement of the increased tumor necrosis factor alpha expression found upon PFOA treatment in reducing the insulin sensitivity of adipose tissue and thereby altering LPL and HSL activities is discussed. Paper-9409172.
The mobilization of fat stored in adipose tissue is mediated by hormone-sensitive lipase ( HSL) and the recently characterized adipose triglyceride lipase ( ATGL), yet their relative importance in lipolysis is unknown. Paper-11527508.
Recombinant human tumor necrosis factor ( TNF) depressed the activities of both lipoprotein lipase ( LPL) and hormone sensitive lipase ( HSL) in 3T3-L1 adipocytes, 3 to 24 h after its introduction to the cells. Paper-6665289.
Adenoviral-mediated expression of Peri A in ACS1/ FATP1 cells enhanced TG accumulation and inhibited lipolysis, whereas expression of HSL fused to green fluorescent protein (GFPHSL) reduced TG accumulation and enhanced lipolysis. Paper-9157366.
However, the mRNA levels of carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP2), as well as lipolytic genes such as hormone sensitive lipase ( HSL) and adipose triglyceride lipase ( ATGL), were significantly increased. Paper-14535752.
This study suggests a direct functional role for both HSL and ATGL in hepatic lipid homeostasis and identifies these enzymes as potential therapeutic targets for ameliorating hepatic steatosis associated with insulin resistance and obesity. Paper-14315459.
Activation of cyclic AMP-dependent protein kinase (PKA) results in the phosphorylation of Peri A and hormone-sensitive lipase ( HSL), the predominant lipase in adipocytes, with concurrent stimulation of adipocyte lipolysis. Paper-9157366.
During fasting, when HSL is normally strongly induced in AT, HSL-ko animals exhibited markedly decreased plasma concentrations of NEFA (-40%) and TG (-63%), whereas total cholesterol and HDL cholesterol levels were increased (+34%). Paper-9159903.
Taken together, our study shows that Kochujang decreased lipid accumulation in 3T3-L1 adipocytes by inhibiting adipogenesis through down-regulation of SREBP-1c and PPAR-gamma and by stimulation of lipolysis due to increased HSL activity. Paper-11311242.
Eight-weeks of HFD feeding increased adipose triglyceride lipase ( ATGL) content and comparative gene identification-58 (CGI-58) expression, whereas hormone-sensitive lipase ( HSL) phosphorylation and perilipin content were severely reduced. Paper-14683332.
Mechanistic studies in oleate-supplemented McA-RH7777 cells with adenoviral overexpression of HSL or ATGL showed that reduced cellular triglycerides could be attributed to increases in beta-oxidation as well as direct release of free fatty acids into the medium. Paper-14315459.
In this study, we demonstrate that adipose triglyceride lipase ( ATGL) and hormone-sensitive lipase ( HSL) are the major enzymes contributing to TG breakdown in in vitro assays and in organ cultures of murine white adipose tissue (WAT). Paper-12365744.
Adrenal glands were enlarged in proportion to the degree of reduced neutral cholesterol ester hydrolase activity, and the enlargement of adrenal glands and the accumulation of cholesterol esters were most pronounced in the Nceh1/ Lipe double-deficient mice. Paper-15609049.
Now, we show that HSL is basally associated with lipid droplet surfaces at a low level in perilipin nulls, but that stimulated translocation from the cytosol to lipid droplets is absent in adipocytes derived from embryonic fibroblasts of perilipin-null mice. Paper-9661828.
Lep(ob/ob)/HSL(-/-) developed elevated blood glucose levels and reduced plasma insulin levels compared with Lep(ob/ob)/HSL(+/+) in a fed state, while the deficiency of HSL did not affect glucose homeostasis in Lep(+/+) background. Paper-13930601.
We go on to show that increases in Id2 can have functional effects on metabolic genes, because Id2 blocked the SREBP-1- induced induction of hormone-sensitive lipase ( HSL) promoter activity, whereas Id2 alone does not modulate activity of the HSL promoter. Paper-11325822.
Because HSL- mediated lipolysis of TG in adipose tissue (AT) directly feeds non-esterified fatty acids (NEFA) into the vascular system, the enzyme is expected to affect many metabolic processes including the metabolism of plasma lipids and lipoproteins. Paper-9159903.
However, in the presence of high glucose both insulin and leptin caused a significant increase in the activity of acyl-CoA: cholesterol O-acyltransferase (ACAT) combined with a significant reduction in the level of hormone-sensitive lipase ( HSL). Paper-9296408.
However, in the presence of 10 microm oleate, A-FABP and E-FABP each bound to HSL with high affinity (Kd of 0.5 and 3 nM, respectively) in a approximately 1:1 molar stoichiometry, whereas liver FABP and intestinal FABP did not exhibit any association. Paper-10041282.
By coexpressing HSL with truncation mutations of Plin, we demonstrate using coimmunoprecipitation that HSL can interact with an N-terminal region located between amino acids 141 and 200 of Plin A as well as with a C-terminal region located between amino acids 406 and 480. Paper-14120421.
Peri 301-517 promoted PKA- stimulated lipolysis by HSL yet did not block HSL-mediated basal lipolysis, indicating that an additional region(s) within Peri 301-517 promotes hormone- stimulated lipolysis by HSL. Paper-10066745.
CGI-58, a recently identified coactivator of ATGL, stimulates TG hydrolase activity in wild-type and HSL-deficient WAT but not in ATGL-deficient WAT, suggesting that ATGL is the sole target for CGI-58-mediated activation of adipose lipolysis. Paper-12365744.
RESULTS: Activation of mTORC1 signaling in 3T3-L1 adipocytes by ectopic expression of Rheb inhibits expression of ATGL and HSL at the level of transcription, suppresses lipolysis, increases de novo lipogenesis, and promotes intracellular accumulation of triglycerides. Paper-14690010.
Currently, three enzymes are known to hydrolyze TG, the well-studied hormone-sensitive lipase ( HSL) and monoglyceride lipase ( MGL), discovered more than 40 years ago, as well as the relatively recently identified adipose triglyceride lipase ( ATGL). Paper-13494305.
RESULTS: JTP-426467 inhibited the expression of hormone-sensitive lipase ( HSL) mRNA, an adipocyte-abundant gene, but not PPARgamma itself or cyclophilin mRNA (as constitutive mRNA), and also suppressed triglyceride accumulation in differentiated stromal vascular fraction cells (SVFs). Paper-12184109.
To test the hypothesis that HSL is involved in control of normal GSIS via changes in its expression and/or activity in response to stimuli, we examined the effects of free fatty acid (FFA) loading and glucagon like peptide-1 ( GLP-1) stimulation on the regulation of HSL expression and activity. Paper-12373668.
To investigate the relative contributions of Peri A and HSL in basal and PKA-mediated lipolysis, we utilized NIH 3T3 fibroblasts lacking Peri A and HSL but stably overexpressing acyl-CoA synthetase 1 ( ACS1) and fatty acid transport protein 1 ( FATP1). Paper-9157366.
Hormone-sensitive lipase ( HSL) is expressed predominantly in white and brown adipose tissue where it is believed to play a crucial role in the lipolysis of stored triglycerides ( TG), thereby providing the body with energy substrate in the form of free fatty acids ( FFA). Paper-9155774.
To identify domains of Peri A that mediate these multiple actions, we introduced adenoviruses expressing truncated or mutated Peri A and HSL into NIH 3T3 fibroblasts lacking endogenous perilipins and HSL but overexpressing acyl-CoA synthetase 1 and fatty acid transporter 1. Paper-10066745.
1. The effects of two chronic ethanol treatment schedules, which produce different plasma ethanol concentrations, on the specific activities of adipose tissue lipoprotein lipase ( LPL) and hormone-sensitive lipase ( HSL) have been investigated in brown and white fat. Paper-993115.
In this study, we have demonstrated that hormone-sensitive lipase ( HSL) and adipose triglyceride lipase ( ATGL), two enzymes critical for lipolysis in adipose tissues, also contribute to lipolysis in the liver and can mobilize hepatic triglycerides in vivo and in vitro. Paper-14315459.
The interaction of HSL with vimentin, and its hormonal dependence, was confirmed by coimmunoprecipitation. beta-Agonist stimulated lipolysis and the rate of HSL translocation were impaired in vimentin null adipocytes, even though normal amounts of lipases and droplet-associated proteins are expressed. Paper-14695726.
In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARalpha agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARalpha. Paper-13454379.
Perilipin ( Peri) A is a lipid droplet-associated phosphoprotein that acts dually as a suppressor of basal (constitutive) lipolysis and as an enhancer of cyclic AMP-dependent protein kinase (PKA)- stimulated lipolysis by both hormone-sensitive lipase ( HSL) and non-HSL(s). Paper-10066745.
A role for glucagon-like peptide 1 ( GLP-1) has been suggested in stimulating beta-cell lipolysis via elevation of cAMP and activation of protein kinase A, which in turn may activate hormone-sensitive lipase ( HSL), thereby contributing to fatty acid generation (FFA) from intracellular triglyceride stores. Paper-11580815.
Studies addressing how Peri A PKA sites regulate adipocyte lipolysis have relied on non-adipocyte cell models, which express neither adipose triglyceride lipase ( ATGL), the rate-limiting enzyme for triglyceride catabolism in mice, nor the "downstream" lipase, hormone-sensitive lipase ( HSL). Paper-12395121.
Because ACAT is the main enzyme responsible for cholesterol ester synthesis and HSL contributes significantly to neutral cholesterol ester hydrolase activity, this suggests that glucose primes the J774.2 cells so that in the presence of high insulin or leptin they will store cholesterol esters. Paper-9296408.
The enhanced adipose tissue hormone-sensitive lipase ( HSL) activity and down-regulated lipoprotein lipase ( LPL) activity observed upon PP treatment might, at least in part, explain the loss of fat via increased FA release from adipocytes and/or decreased FA uptake from the circulation, respectively. Paper-9409172.
To differentiate between ATGL- and HSL-specific activities in cytosolic preparations of WAT and to determine the relative contribution of these TG hydrolases to the lipolytic catabolism of fat, mutant mouse models lacking ATGL or HSL and a mono-specific, small molecule inhibitor for HSL (76-0079) were used. Paper-12365744.
RESEARCH DESIGN AND METHODS: In this study, we analyzed the effect of activation and inhibition of the mammalian TORC1 (mTORC1) signaling pathway on the expression of adipose triglyceride lipase ( ATGL), hormone-sensitive lipase ( HSL), lipolysis, lipogenesis, and lipid storage in different mammalian cells. Paper-14690010.
Moreover, in Chinese hamster ovary cells that express both HSL and perilipin A, these two proteins cooperate to produce a more rapidly accelerated lipolysis than do cells that express either of these proteins alone, indicating that lipolysis is a concerted reaction mediated by both protein kinase A-phosphorylated HSL and perilipin A. Paper-9661828.
These observations suggest that the high level of steroid biosynthesis in R2C cells is a result of the constitutive expression of the components involved in the uptake of cholesterol esters ( SR-B1), their conversion to free cholesterol ( HSL), and its mobilization to the inner mitochondrial membrane ( StAR). Paper-9767042.
Studies with ATGL-and HSL-directed small hairpin RNAs demonstrate that 1) ATGL activity is required for all PKA-stimulated FA and glycerol release in murine embryonic fibroblast adipocytes and 2) all PKA-stimulated FA release in the absence of HSL activity requires serine 517 phosphorylation. Paper-12395121.
We identified two lipase-selective functional domains: 1) Peri A (amino acids 1-300), which inhibits basal lipolysis and promotes PKA-stimulated lipolysis by HSL, and 2) Peri A (amino acids 301-517), which inhibits basal lipolysis by non- HSL and promotes PKA-stimulated lipolysis by both HSL and non- HSL. Paper-10066745.
The phenotype of HSL- and ATGL-deficient mice, as well as the disease pattern of patients with defective ATGL activity (due to mutation in ATGL or in the enzyme's activator, CGI-58), suggest that the consecutive action of ATGL, HSL, and MGL is responsible for the complete hydrolysis of a TG molecule. Paper-13494305.
This work examined the mechanisms by which activation of hormone sensitive lipase ( HSL) induces expression of inflammatory cytokines in adipocytes in vivo and model adipocytes in vitro. beta3-AR activation in mice triggered expression of inflammatory genes CCL2, IL-6, and PAI-1, as well as endoplasmic reticulum (ER) stress markers GRP78 and CHOP. Paper-15215987.
AIMS/HYPOTHESIS: The recent identification of murine adipose triglyceride lipase ( ATGL, now known as patatin-like phospholipase domain containing 2 [ PNPLA2]), gene product of Pnpla2, has questioned the unique role of hormone sensitive lipase ( HSL, now known as LIPE), gene product of Lipe, in fat cell lipolysis. Paper-12117226.
We have previously demonstrated that neutral cholesterol ester hydrolase 1 ( Nceh1) regulates foam cell formation and atherogenesis through the catalytic activity of cholesterol ester hydrolysis, and that Nceh1 and hormone-sensitive lipase ( Lipe) are responsible for the majority of neutral cholesterol ester hydrolase activity in macrophages. Paper-15609049.
In addition to the previously demonstrated increased expression of StAR protein, we show that R2C cells possess marginally enhanced protein kinase A activity, exhibit higher capacity to take up extracellular cholesterol esters, and express much higher levels of scavenger receptor-type B class 1 ( SR-B1) and hormone sensitive lipase ( HSL). Paper-9767042.
From these data we conclude that 1) macrophages release a cytokine(s) in response to lipopolysaccharide that stimulates lipolysis in freshly isolated adipocytes; 2) TNF alpha can account for most, or perhaps all, of this effect; 3) TNF alpha increases the rate of lipolysis by a mechanism that does not involve increased expression of HSL. Paper-121665.
Increases in mRNA expression were found for hormone sensitive lipase ( HSL), uncoupling protein 2 (UCP2), adrenergic receptor 3 (ADR3), mitofusin 2 (Mfn2), sirtuin 3 (Sirt3), transcription factor sterol regulatory element binding factor 1 (SREBF1), Bcl-2, Bax, Caspase 3, tumor necrosis factor alpha ( TNFalpha), adiponectin and angiopoietin 2 ( Ang-2). Paper-12849709.
These synonyms are used for gene Lipe (lipase, hormone sensitive): HSL, Hormone-sensitive lipase, 4933403G17Rik.
These accession numbers are used for gene Lipe: Q6GU16 (UNIPROT__AC), P97866 (UNIPROT__AC), BC021642 (NCBI_GENBANK__AC), AK169858 (NCBI_GENBANK__AC).
Lipe is a homologue of LIPE (lipase, hormone-sensitive) from Homo sapiens.
Lipe is a homologue of LIPE (lipase, hormone-sensitive) from Canis lupus familiaris.
Lipe is a homologue of LIPE (lipase, hormone-sensitive) from Bos taurus.
Lipe is a homologue of Lipe (lipase, hormone sensitive) from Rattus norvegicus.
Lipe is a homologue of lipe (lipase, hormone-sensitive) from Danio rerio.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.