Exercise restores insulin, but not adiponectin, response in skeletal muscle of high-fat fed rodents

摘要

Since the discoveries of leptin and adiponectin (Ad), a growing body of evidence has linked these adipose tissue-derived hormones (adipokines) to changes in skeletal muscle FA oxidation, reactive lipid species accumulation, and insulin resistance (29, 32, 37, 39). In isolated skeletal muscle from both rodents and humans, these adipokines promote FA oxidation rather than storage, a purportedly protective effect (7). These adipokines stimulate AMPK in skeletal muscle (19, 36), which, in turn, phosphorylate ACC, leading to an increase in FA oxidation (32). Ad stimulation of this cascade is regulated by its surface receptors AdipoRl and AdipoR2 (with AdipoRl being the predominant muscle isoform) and adaptor proteins APPL1 and APPL2 (33).