ArticleMetabolism: clinical and experimental2019
Ectopic lipid deposition mediates insulin resistance in adipose specific 11β-hydroxysteroid dehydrogenase type 1 transgenic mice.
Article in Metabolism: clinical and experimental, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 22 citations in OpenAlex.
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- Strength Training Protects High-Fat-Fed Ovariectomized Mice against Insulin Resistance and Hepatic Steatosis.International journal of molecular sciences · 2024Article
- Differences in diacylglycerol acyltransferases expression patterns and regulation cause distinct hepatic triglyceride deposition in fish.Communications biology · 2024Article
- Excessive Daytime Napping Increases the Risk of Non-Alcoholic Fatty Liver Disease: A Meta-Analysis and a Mendelian Randomization Study.Nature and science of sleep · 2024Article
- Bioactive lipids and metabolic syndrome-a symposium report.Annals of the New York Academy of Sciences · 2022Article
- Positive association of nap duration with risk of non-alcoholic fatty liver disease in an occupational population in Guangdong Province, China: a cross-sectional study.BMC gastroenterology · 2022Article
- Sex- and strain-specific effects of mitochondrial uncoupling on age-related metabolic diseases in high-fat diet-fed mice.Aging cell · 2022Article
- Membrane-boundJournal of lipid research · 2020Article
- Glucocorticoid-Induced Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- Quantification of Multi-Organ 11β-Hydroxysteroid Dehydrogenase Type 1 Enzyme Levels in a Zucker Fatty Rat Model: A PET Imaging Study.Molecular imagingArticle
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6 authors at 1 institution in 1 country.
Funding
Abstract
contextExcessive adipose glucocorticoid action is associated with insulin resistance, but the mechanisms linking adipose glucocorticoid action to insulin resistance are still debated. We hypothesized that insulin resistance from excess glucocorticoid action may be attributed in part to increased ectopic lipid deposition in liver.
methodsWe tested this hypothesis in the adipose specific 11β-hydroxysteroid dehydrogenase-1 (HSD11B1) transgenic mouse, an established model of adipose glucocorticoid excess. Tissue specific insulin action was assessed by hyperinsulinemic-euglycemic clamps, hepatic lipid content was measured, hepatic insulin signaling was assessed by immunoblotting. The role of hepatic lipid content was further probed by administration of the functionally liver-targeted mitochondrial uncoupler, Controlled Release Mitochondrial Protonophore (CRMP).
findingsHigh fat diet fed HSD11B1 transgenic mice developed more severe hepatic insulin resistance than littermate controls (endogenous suppression of hepatic glucose production was reduced by 3.8-fold, P < 0.05); this was reflected by decreased insulin-stimulated hepatic insulin receptor kinase tyrosine phosphorylation and AKT serine phosphorylation. Hepatic insulin resistance was associated with a 53% increase (P < 0.05) in hepatic triglyceride content, a 73% increase in diacylglycerol content (P < 0.01), and a 66% increase in PKCε translocation (P < 0.05). Hepatic insulin resistance was prevented with administration of CRMP by reversal of hepatic steatosis and prevention of hepatic diacylglycerol accumulation and PKCε activation.
conclusionsThese findings are consistent with excess adipose glucocorticoid activity being a predisposing factor for the development of lipid (diacylglycerol-PKCε)-induced hepatic insulin resistance.
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