ArticleJournal of atherosclerosis and thrombosis2017
Role of Hormone-sensitive Lipase in Leptin-Promoted Fat Loss and Glucose Lowering.
Article in Journal of atherosclerosis and thrombosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Tissue-Specific Effects of Leptin on Glucose and Lipid Metabolism.Endocrine reviews · 2021Review
- Critical Role of SREBP-1c Large-VLDL Pathway in Environment-Induced Hypertriglyceridemia of Apo AV Deficiency.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Leptin Resistance and Lipolysis of White Adipose Tissue: An Implication to Ectopic Fat Disposition and Its Consequences.Journal of atherosclerosis and thrombosis · 2017Article
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Authors and funding
18 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimMyriad biological effects of leptin may lead to broad therapeutic applications for various metabolic diseases, including diabetes and its complications; however, in contrast to its anorexic effect, the molecular mechanisms underlying adipopenic and glucose-lowering effects of leptin have not been fully understood. Here we aim to clarify the role of hormone-sensitive lipase (HSL) in leptin's action.
methodsWild-type (WT) and HSL-deficient (HSLKO) mice were made hyperleptinemic by two commonly-used methods: adenovirus-mediated overexpression of leptin and continuous subcutaneous infusion of leptin by osmotic pumps. The amount of food intake, body weights, organ weights, and parameters of glucose and lipid metabolism were measured.
resultsHyperleptinemia equally suppressed the food intake in WT and HSLKO mice. On the other hand, leptin-mediated fat loss and glucose-lowering were significantly blunted in the absence of HSL when leptin was overexpressed by recombinant adenovirus carrying leptin. By osmotic pumps, the fat-losing and glucose-lowering effects of leptin were milder due to lower levels of hyperleptinemia; although the difference between WT and HSLKO mice did not reach statistical significance, HSLKO mice had a tendency to retain more fat than WT mice in the face of hyperleptinemia.
conclusionsWe clarify for the first time the role of HSL in leptin's effect using a genetic model: leptin-promoted fat loss and glucose-lowering are at least in part mediated via HSL-mediated lipolysis. Further studies to define the pathophysiological role of adipocyte lipases in leptin action may lead to a new therapeutic approach to circumvent leptin resistance.
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