Induction of glucose uptake in skeletal muscle by central leptin is mediated by muscle β2-adrenergic receptor but not by AMPK View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Tetsuya Shiuchi, Chitoku Toda, Shiki Okamoto, Eulalia A. Coutinho, Kumiko Saito, Shinji Miura, Osamu Ezaki, Yasuhiko Minokoshi

ABSTRACT

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. More... »

PAGES

15141

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-017-15548-6

DOI

http://dx.doi.org/10.1038/s41598-017-15548-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1092523053

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29123236


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279 Second Department of Internal Medicine (Endocrinology, Diabetes and Metabolism, Hematology, Rheumatology), Graduate School of Medicine, University of the Ryukyus, 903-0215, Okinawa, Japan
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282 schema:name Department of Physiological Sciences, School of Life Sciences, SOKENDAI (The Graduate University for Advanced Studies), 444-8585, Okazaki, Aichi, Japan
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286 schema:name Centre for Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago, 9054, Dunedin, New Zealand
287 Department of Physiological Sciences, School of Life Sciences, SOKENDAI (The Graduate University for Advanced Studies), 444-8585, Okazaki, Aichi, Japan
288 Division of Endocrinology and Metabolism, Department of Homeostatic Regulation, National Institute for Physiological Sciences, National Institutes of Natural Sciences, 444-8585, Okazaki, Aichi, Japan
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291 schema:name Division of Endocrinology and Metabolism, Department of Homeostatic Regulation, National Institute for Physiological Sciences, National Institutes of Natural Sciences, 444-8585, Okazaki, Aichi, Japan
292 Laboratory of Biochemistry, Graduate School of Veterinary Medicine, Hokkaido University, 060-0818, Sapporo, Japan
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294 https://www.grid.ac/institutes/grid.412583.9 schema:alternateName Showa Women's University
295 schema:name Department of Human Health and Design, Showa Women’s University, 154-8533, Tokyo, Japan
296 Nutritional Science Program, National Institute of Health and Nutrition, 162-8636, Tokyo, Japan
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302 schema:name Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, 422-8526, Shizuoka, Japan
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