内科学
胰岛素抵抗
内分泌学
脂肪变性
葡萄糖稳态
过剩2
平衡
生物
脂滴
胆汁酸
化学
胰岛素
葡萄糖转运蛋白
医学
作者
Wanying Qin,Ting Zhang,Ming-Xia Ge,Huimin Zhou,Yuhui Xu,Rong‐Fang Mu,Chao-Guang Huang,Daowei Liu,Bangrui Huang,Qian Wang,Qinghua Kong,Qing‐Peng Kong,Fēi Li,Wenyong Xiong
摘要
Receptor for activated C kinase 1 (RACK1) is a versatile protein involved in multiple biological processes. In a previous study by Zhao et al. , hepatic RACK1 deletion in mice led to an inhibition of autophagy, blocked autophagy-dependent lipolysis, and caused steatosis. Using the same mouse model (RACK1 hep−/− ), we revealed new roles of RACK1 in maintaining bile acid homeostasis and hepatic glucose uptake, which further affected circulatory lipid and glucose levels. To be specific, even under hepatic steatosis, the plasma lipids were generally reduced in RACK1 hep−/− mouse, which was due to the suppression of intestinal lipid absorption. Accordingly, a decrease in total bile acid level was found in RACK1 hep−/− livers, gallbladders, and small intestine tissues, and specific decrease of 12-hydroxylated bile acids was detected by liquid chromatography–mass spectrometry. Consistently, reduced expression of CYP8B1 was found. A decrease in hepatic glycogen storage was also observed, which might be due to the inhibited glucose uptake by GLUT2 insufficiency. Interestingly, RACK1-KO-inducing hepatic steatosis did not raise insulin resistance (IR) nor IR-inducing factors like endoplasmic reticulum stress and inflammation. In summary, this study uncovers that hepatic RACK1 might be required in maintaining bile acid homeostasis and glucose uptake in hepatocytes. This study also provides an additional case of hepatic steatosis disassociation with insulin resistance.
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