志内, 哲也 National Institutes of Natural Sciences|SOKENDAI (The Graduate University for Advanced Studies)|Tokushima University 徳島大学 教育研究者総覧 KAKEN研究者をさがす
Toda, Chitoku National Institutes of Natural Sciences|Hokkaido University
Okamoto, Shiki National Institutes of Natural Sciences|SOKENDAI (The Graduate University for Advanced Studies)|University of the Ryukyus
Coutinho, Eulalia A. National Institutes of Natural Sciences|SOKENDAI (The Graduate University for Advanced Studies)|University of Otago
Saito, Kumiko National Institutes of Natural Sciences
Miura, Shinji National Institute of Health and Nutrition|University of Shizuoka
Ezaki, Osamu National Institute of Health and Nutrition|Showa Women’s University
Minokoshi, Yasuhiko National Institutes of Natural Sciences|SOKENDAI (The Graduate University for Advanced Studies)
Leptin increases glucose uptake and fatty acid oxidation (FAO) in red-type skeletal muscle. However, the mechanism remains unknown. We have investigated the role of β2-adrenergic receptor (AR), the major β-AR isoform in skeletal muscle, and AMPK in leptin-induced muscle glucose uptake of mice. Leptin injection into the ventromedial hypothalamus (VMH) increased 2-deoxy-D-glucose (2DG) uptake in red-type skeletal muscle in wild-type (WT) mice accompanied with increased phosphorylation of the insulin receptor (IR) and Akt as well as of norepinephrine (NE) turnover in the muscle. Leptin-induced 2DG uptake was not observed in β-AR-deficient (β-less) mice despite that AMPK phosphorylation was increased in the muscle. Forced expression of β2-AR in the unilateral hind limb of β-less mice restored leptin-induced glucose uptake and enhancement of insulin signalling in red-type skeletal muscle. Leptin increased 2DG uptake and enhanced insulin signalling in red-type skeletal muscle of mice expressing a dominant negative form of AMPK (DN-AMPK) in skeletal muscle. Thus, leptin increases glucose uptake and enhances insulin signalling in red-type skeletal muscle via activation of sympathetic nerves and β2-AR in muscle and in a manner independent of muscle AMPK.
Supplementary Information : srep_7_15141_s1.pdf
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