ID 112436
Author
Shiuchi, Tetsuya National Institutes of Natural Sciences|SOKENDAI (The Graduate University for Advanced Studies)|Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
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)
Content Type
Journal Article
Description
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.
Journal Title
Scientific Reports
ISSN
20452322
Publisher
Springer Nature
Volume
7
Start Page
15141
Published Date
2017-11-09
Remark
Supplementary Information : srep_7_15141_s1.pdf
Rights
© The Author(s) 2017
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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language
eng
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departments
Medical Sciences