| First Author | Shiuchi T | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 15141 |
| PubMed ID | 29123236 | Mgi Jnum | J:257269 |
| Mgi Id | MGI:6110503 | Doi | 10.1038/s41598-017-15548-6 |
| Citation | Shiuchi T, et al. (2017) Induction of glucose uptake in skeletal muscle by central leptin is mediated by muscle beta2-adrenergic receptor but not by AMPK. Sci Rep 7(1):15141 |
| abstractText | 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 beta2-adrenergic receptor (AR), the major beta-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 beta-AR-deficient (beta-less) mice despite that AMPK phosphorylation was increased in the muscle. Forced expression of beta2-AR in the unilateral hind limb of beta-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 beta2-AR in muscle and in a manner independent of muscle AMPK. |
