Chronic palmitate exposure inhibits AMPKalpha and decreases glucose-stimulated insulin secretion from beta-cells: modulation by fenofibrate.
作者
Sun Ying;Ren Meng;Gao Guan-qi;Gong Bendi;Xin Wei;Guo Hua;Zhang Xiu-juan;Gao Ling;Zhao Jia-ju
作者单位
摘要
Adenosine monophosphate-activated protein kinase (AMPK), a vital regulator of glucose metabolism, may affect insulin secretion in beta-cells. However, the role of AMPK in beta-cell lipotoxicity remains unclear. Fenofibrate has been reported to regulate lipid homeostasis and is involved in insulin secretion in pancreatic beta-cells. In the present study, we aimed to investigate the effect of palmitate on AMPK expression and glucose-stimulated insulin secretion (GSIS) in rat islets and INS-1 beta-cell, as well as the effect of fenofibrate on AMPK and GSIS in INS-1 cells treated with palmitate.
关键词
AMP-Activated Protein Kinases/antagonists & inhibitors|Animals|Cell Culture Techniques|Cell Line, Tumor|Cells, Cultured|Dose-Response Relationship, Drug|Fenofibrate/pharmacology|Glucose/pharmacology|Insulin/secretion|Insulin-Secreting Cells/drug effects/metabolism|Insulinoma/metabolism|Islets of Langerhans/cytology/drug effects/physiology|Luminescence|Luminescent Measurements|Male|PPAR alpha/metabolism|Palmitates/pharmacology|Rats|Rats, Wista
基本信息
