期刊
CELL
卷 165, 期 3, 页码 566-579出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.02.063
关键词
-
资金
- Baylor-Johns Hopkins Center for Mendelian Genomics [U54HG006542]
- NHGRI [U54HG006542]
- Mouse Metabolic Core at BCM
- NIH [P30 DK079638, P50 HL083794, DK059637, DK020593]
- Thoracic Aortic Disease Tissue Bank at BCM
- NCI
- NHGRI
- NHLBI
- NIDA
- NIMH
- NINDS
- NIDDK [1K08DK102529]
- Chao Physician-Scientist Award
- Caroline Weiss Law scholar award
Hepatic glucose release into the circulation is vital for brain function and survival during periods of fasting and is modulated by an array of hormones that precisely regulate plasma glucose levels. We have identified a fasting-induced protein hormone that modulates hepatic glucose release. It is the C-terminal cleavage product of profibrillin, and we name it Asprosin. Asprosin is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. Humans and mice with insulin resistance show pathologically elevated plasma asprosin, and its loss of function via immunologic or genetic means has a profound glucose- and insulin-lowering effect secondary to reduced hepatic glucose release. Asprosin represents a glucogenic protein hormone, and therapeutically targeting it may be beneficial in type II diabetes and metabolic syndrome.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据