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- W1976100963 abstract "The adipocyte-derived hormone adiponectin was recently shown to stimulate glucose-utilization and to increase fatty acid oxidation in liver and muscle. The effects were ascribed to adiponectin-receptor mediated activation of the key metabolic regulator AMP-activated protein kinase (AMPK). In pancreatic beta cells, AMPK-activation is known to affect cellular function. We therefore investigated a possible adiponectin-induced activation of AMPK in beta cells. RT-PCR analysis confirmed the expression of adiponectin receptor subtypes 1 and 2 in rat beta cells and showed their expression in insulin-secreting MIN6 cells. Culture with physiological concentrations (2.5 μg/ml) of globular adiponectin was found to increase the phosphorylation of both AMPK and acetylcoA carboxylase (ACC) in these cell types. Like the pharmacological AMPK activator 5-amino-imidazole-4-carboxamide-riboside (AICAR), adiponectin activated AMPK in beta cells and MIN6 cells. In short-term incubations of MIN6 cells with either adiponectin (2.5 μg/ml) or AICAR (1 mM), the flux of glucose-carbon to acyl CoA/cholesterol biosynthetic intermediates was reduced. We conclude that adiponectin induces an activation of AMPK in beta cells, which inhibits their cataplerosis of glucose-carbon to lipids." @default.
- W1976100963 created "2016-06-24" @default.
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- W1976100963 date "2005-07-01" @default.
- W1976100963 modified "2023-10-02" @default.
- W1976100963 title "Adiponectin-mediated stimulation of AMP-activated protein kinase (AMPK) in pancreatic beta cells" @default.
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- W1976100963 doi "https://doi.org/10.1016/j.lfs.2005.03.008" @default.
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