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The homozygous null LIPE mutation could result in marked inhibition of lipolysis from some adipose tissue depots and thus may induce an extremely rare phenotype of MSL and partial lipodystrophy in adulthood associated with complications of insulin (show INS Proteins) resistance, such as diabetes, hypertriglyceridemia and hepatic steatosis.
Despite reductions in intramyocellular lipolysis and HSL expression, overexpression of HSL did not rescue defects in insulin (show INS Proteins) action in skeletal myotubes from obese type 2 diabetic subjects.
Identification of a homozygous nonsense variant p.Ala507fsTer563 in hormone sensitive lipase as the likely cause of the lipodystrophy phenotype in siblings.
These findings indicate the physiological significance of HSL in adipocyte function and the regulation of systemic lipid and glucose homeostasis and underscore the severe metabolic consequences of impaired lipolysis.
Serum triglyceride was significantly up-regulated in men with the (CG + GG) genotype of HSL promoter polymorphism.
M. leprae suppresses lipid degradation through inhibition of HSL expression.
Enzyme promiscuity in the hormone-sensitive lipase family of proteins.
Resveratrol increased adipose triglyceride lipase (show PNPLA2 Proteins) gene and protein expressions, an effect that was not observed for hormone-sensitive lipase in human SGBS adipocytes.
LIPE C-60G variation can inhibit the decrease of LDL-C and the increases of HDL (show HSD11B1 Proteins)-C and apo A (show APOA Proteins)-I in young healthy males, and can inhibit the decrease of LDL-C and the increase of insulin (show INS Proteins) in young healthy females induced by a high-carbohydrate diet.
suggests that genetic variation of HSL may be a risk factor for male infertility
Polymorphisms in HSL might be one of important genetic factors that influence carcass yield and meat quality in beef cattle.
These results suggest that HSL was regulated by fatty acids and some hormones in mammary epithelial cells and thereby play an important role of lipid and energy metabolism.
HSL-deficient mice revealed a complex interorgan interaction between adipose tissue and liver: the role of HSL in the liver is minimal but adipose tissue deficiency of HSL can cause age-dependent hepatic steatosis
Cardiac PLIN2 (show PLIN2 Proteins) plays an important pathophysiological role in the development of dynamic steatosis and that the latter was prevented by upregulation of intracellular lipases, including Hormone-sensitive Lipase.
Enhanced lipolysis in response to mitochondrial uncoupling relies on a form of autophagy as lipid droplets are captured by endolysosomal vesicles which is HSL/ATGL (show PNPLA2 Proteins)-independent.
HSL ablation alters the density of lipid-raft microdomains in mouse testis. HSL-/- lipid rafts had less desmosterol and T-MAS (show MAS1 Proteins); non-raft had more cholesterol.Monounsaturated acyl phospholipids were higher in raft than in non-raft fractions.HSL ablation reduced PUFA-phospholipids in both raft and non-raft fractions.
ase (show ARSE Proteins). Similar changes of GPNMB and G0S2 (show G0S2 Proteins) expression were present in a human liposarcoma database. These results show that a previously-unknown, fully penetrant epistatic interaction between Pnpla2 (show PNPLA2 Proteins) and Lipe can cause liposarcoma in mice. DAKO mice provide a promising model for studying early premalignant changes that lead to late-onset malignant disease.
Activities of adipose triglyceride lipase (ATGL (show PNPLA2 Proteins)), hormone sensitive lipolitic enzyme (HSL) and monoacylglycerol lipase (MGL (show MGLL Proteins)) were significantly higher (51 %, 38 %, 49 %) in the DE group than the HF group (p < 0.05). MGL (show CLEC10A Proteins), there were no differences between the CO group, HF group, and DC group, with the DE group (70 %) being significantly higher (p < 0.05).
Results clearly indicate that SF-1 (show SF1 Proteins) is involved in the regulation of LIPE expression after activation of protein kinase A in adrenocortical cells.
A role for HSL in kidney lipolysis:fasting up-regulates HSL levels and phosphorylation in mouse kidney.
Data suggest that cardiotrophin-1 (show CTF1 Proteins) up-regulates lipolysis in white adipocytes via 1) induction of perilipin (show PLIN1 Proteins), 2) activation of HSL (via phosphorylation by PKA), and 3) inactivation of adipose triglyceride lipase (show PNPLA2 Proteins) (via up-regulation of inhibitor G0S2 (show G0S2 Proteins)).
QRFP-43 attenuates lipolysis by preventing the formation of an active complex between perilipin A (show PLIN1 Proteins), caveolin-1 (show CAV1 Proteins), the catalytic subunit of protein kinase (show CDK7 Proteins) and hormone-sensitive lipase on lipid droplets.
The protein encoded by this gene has a long and a short form, generated by use of alternative translational start codons. The long form is expressed in steroidogenic tissues such as testis, where it converts cholesteryl esters to free cholesterol for steroid hormone production. The short form is expressed in adipose tissue, among others, where it hydrolyzes stored triglycerides to free fatty acids.
, hormone-sensitive lipase testicular isoform
, hormone - sensitive lipase testicular isoform
, lipase E
, lipase, hormone-sensitive
, hormone-sensitive lipase-like
, CG11055 gene product from transcript CG11055-RB
, Hormone-sensitive lipase ortholog
, hormone sensitive lipase
, transcription unit A