期刊
BIOCHEMICAL PHARMACOLOGY
卷 156, 期 -, 页码 241-247出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2018.08.036
关键词
GALR2; Intracerebroventricular injection; Glucose metabolism; PGC-1 alpha; GLUT4
资金
- National Natural Scientific Fund of China [81803792]
- National Health and Family Planning Commission of China [W201309]
- Natural Scientific Fund of Jiangsu [BK20171319]
- Science and technology project of Jiangsu Provincial Administration of traditional Chinese Medicine [YB2015138]
- Six talent peaks project in Jiangsu Province [WSN-113]
- Science and Technology Program of Taizhou [TS201723]
Although recent results of our and other studies have showed that galanin (GAL) is an antidiabetic and anti-inflammatory neuropeptide, the molecular mechanism how central GAL regulates energy homeostasis and insulin sensitivity is still not fully understood. The aim of this study was to investigate whether central type 2 of GAL receptors (GALR2) are involved in the regulation of systemic glucose metabolism and its underlying mechanisms. In the present study, type 2 diabetic rats were intracerebroventricularly (i.c.v.) given 100 nM/kg/d GALR2 agonist M1145 or GALR2 antagonist M871 in 5 mu l artificial cerebrospinal fluid once a day for consecutive 21 days. Then insulin resistance indexes, inflammatory factor and many genes associated with the function of glucose metabolism were examined in peripheral tissues. The present findings showed that the intracerebroventricular injection of M1145 or M871 respectively increased or decreased glucose infusion rates in hyperinsulinemic euglycemic clamp tests, but attenuated or enhanced the plasma inflammatory factors and glucose concentration in type 2 diabetic rats. Moreover, administration of M1145 markedly increased PGC-1 alpha and GLUT4 expression in skeletal muscles and adipocytes of type 2 diabetic rats. In conclusion, activation of central GALR2 promotes glucose metabolism and ameliorates insulin resistance mainly through the PGC-1 alpha/GLUT4 pathways. The central GALR2 is crucial to whole-body insulin sensitivity and energy homeostasis.
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