期刊
PEPTIDES
卷 30, 期 6, 页码 1098-1104出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.peptides.2009.03.006
关键词
c-Jun N-terminal kinase (JNK); Melanocortin receptor; AKT; Insulin; Insulin receptor substrate 1 (IRS-1); MT II; NDP-MSH; Hypothalamus
资金
- NIH [DK054032, 5R37DK043225-17]
The melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (INK). The melanocortin agonist NDP-MSH dose-dependently inhibited INK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on INK activity. (C) 2009 Elsevier Inc. All rights reserved.
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