ArticleAmerican journal of physiology. Endocrinology and metabolism2009
Amino acid-sensing mTOR signaling is involved in modulation of lipolysis by chronic insulin treatment in adipocytes.
Article in American journal of physiology. Endocrinology and metabolism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- miR-720 Regulates Insulin Secretion by Targeting Rab35.BioMed research international · 2021Article
- Review
- mTORC1 signaling and the metabolic control of cell growth.Current opinion in cell biology · 2017Review
- Article
- The multifaceted role of mTORC1 in the control of lipid metabolism.EMBO reports · 2013Review
- Hepatitis C virus core protein decreases lipid droplet turnover: a mechanism for core-induced steatosis.The Journal of biological chemistry · 2011Article
- Chronic leucine supplementation improves glycemic control in etiologically distinct mouse models of obesity and diabetes mellitus.Nutrition & metabolism · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Chronically high insulin levels and increased circulating free fatty acids released from adipose tissue through lipolysis are two features associated with insulin resistance. The relationship between chronic insulin exposure and adipocyte lipolysis has been unclear. In the present study we found that chronic insulin exposure in 3T3-L1 adipocytes, as well as in mouse primary adipocytes, increased basal lipolysis rates. This effect of insulin on lipolysis was only observed when the mammalian target of rapamycin (mTOR) pathway was inhibited by rapamycin in the adipocytes. In addition, amino acid deprivation in adipocytes phenocopied the effect of rapamycin in permitting the stimulation of lipolysis by chronic insulin exposure. The phosphatidylinositol 3-kinase-Akt pathway does not appear to be involved in this insulin effect. Furthermore, we found that triacylglycerol hydrolase (TGH) activity was required for the stimulation of lipolysis by combined exposure to insulin and rapamycin. Therefore, we propose that nutrient sufficiency, mediated by an mTOR pathway, suppresses TGH-dependent lipolysis stimulated by chronic insulin exposure in adipocytes.
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Registered trials
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