Endogenous epinephrine protects against obesity induced insulin resistance

被引:12
作者
Ziegler, Michael G. [1 ]
Milic, Milos [1 ]
Sun, Ping [1 ]
Tang, Chih-Min [1 ]
Elayan, Hamzeh [2 ]
Bao, Xuping [1 ]
Cheung, Wai Wilson [1 ]
O'Connor, Daniel T. [1 ]
机构
[1] UCSD, Dept Med, La Jolla, CA 92093 USA
[2] Univ Jordan, Fac Med, Dept Pharmacol, Amman, Jordan
来源
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL | 2011年 / 162卷 / 1-2期
关键词
Phenylethanolamine N-methyltransferase; PNMT; Mouse; Glucose; Diabetes mellitus; MUSCLE; MOUSE; RAT;
D O I
10.1016/j.autneu.2011.01.009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Epinephrine (E) is a hormone released from the adrenal medulla in response to low blood sugar and other stresses. E and related beta 2-adrenergic agonists are used to treat asthma, but a side effect is high blood sugar. C57BL/6 mice prone to overfeeding induced type II diabetes had the PNMT gene knocked out to prevent E synthesis. These E deficient mice were very similar to control animals on a 14% fat diet. On a 40.6% fat diet they gained 20 to 33% more weight than control animals and increased their blood glucose response to a glucose tolerance test because they became resistant to insulin. Although the short term effect of beta 2-agonists such as E is to raise blood glucose, some long acting beta 2-agonists improve muscle glucose uptake. Endogenous E protects against overfeeding induced diabetes. Since adrenal E release can be impaired with aging and diabetes, endogenous E may help prevent adult onset diabetes. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:32 / 34
页数:3
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