胰岛素抵抗
脂肪变性
非酒精性脂肪肝
内分泌学
自噬
内科学
脂质代谢
脂肪肝
下调和上调
碳水化合物代谢
医学
胰岛素
生物
脂滴
细胞凋亡
疾病
生物化学
基因
作者
Ya Liu,Xiaoqing Zhou,Ye Xiao,Changjun Li,Yan Huang,Qi Guo,Tian Su,Ling Fu,Liping Luo
摘要
Nonalcoholic fatty liver disease (NAFLD) is becoming the most prevalent liver disease worldwide, is characterized by liver steatosis and is often accompanied with other pathological features such as insulin resistance. However, the underlying mechanisms are not fully understood, and specific pharmacological agents need to be developed. Here, we investigated the role of microRNA-188 (miR-188) as a negative regulator in hepatic glucose and lipid metabolism. miR-188 was upregulated in the liver of obese mice. Loss of miR-188 alleviated diet-induced hepatosteatosis and insulin resistance. In contrast, liver-specific overexpression of miR-188 aggravated hepatic steatosis and insulin resistance during high-fat diet feeding. Mechanistically, we found that the negative effects of miR-188 on lipid and glucose metabolism were mediated by the autophagy pathway via targeting autophagy-related gene 12 ( Atg12 ). Furthermore, suppressing miR-188 in the liver of obese mice improved liver steatosis and insulin resistance. Taken together, our findings reveal a new regulatory role of miR-188 in glucose and lipid metabolism through the autophagy pathway, and provide a therapeutic insight for NAFLD.
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