Effect and Mechanism of Inhibition Mitochondrial Complex Ⅰ on Glucose Metabolism in Diabetic Mice
10.11969/j.issn.1673-548X.2024.05.017
- VernacularTitle:抑制线粒体复合物Ⅰ对糖尿病小鼠糖代谢的影响及机制
- Author:
Wolin HOU
1
;
Yanyun HU
Author Information
1. 200080 上海交通大学附属第一人民医院老年科
- Keywords:
Mitochondrial complex Ⅰ;
Endoplasmic reticulum stress;
Diabetic mice;
Insulin resistance;
Glucose transporter
- From:
Journal of Medical Research
2024;53(5):80-85
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect and mechanism of mitochondrial complex Ⅰ on glucose metabolism in diabetic mice.Methods The diabetic mouse model was induced by high-fat feeding combined with streptozotocin,and the healthy control group,dia-betic group,and rotenone group were set up.After 6 weeks of intervention,the body weight,daily food intake,fasting blood glucose,in-dex of intraperitoneal injection of glucose tolerance and insulin tolerance,liver and muscle glycogen deposition of mice in each group were detected.Real-time quantitative polymerase chain reaction(RT-qPCR)was used to detect the mRNA expression levels of glucose transporter 1(GLUT1),GLUT2 and GLUT4 of liver and muscle,and Western blot was used to detect the phosphorylation level of eukary-otic translation initiation factor 2α(eIF2α)and the protein expression level of activating transcription factor 4(ATF4).Results Com-pared with the mice in diabetic group,the body weight,blood glucose,area under the curve of intraperitoneal glucose tolerance test(IPGTT)and insulin tolerance test(ITT)of the mice in the rotenone group were significantly decreased,and the liver glycogen reserve was significantly increased.Compared with the healthy control group,the mRNA expression levels of liver GLUT1 and GLUT2,muscle GLUT1 and GLUT4 in the diabetic group were significantly decreased,while the expression of the above GLUT in the rotenone group was significantly higher than that in the diabetic group.Compared with the healthy control group,the protein expression levels of p-eIF2αand ATF4 in the diabetic group were significantly increased,while the expression levels of p-eIF2α and ATF4 in the rotenone group were significantly lower than those in the diabetic group.Conclusion Inhibition of mitochondrial complex Ⅰ may up-regulate the expression of GLUT through the eIF2α/ATF4 signaling pathway,and improve glucose metabolism and insulin resistance in diabetic mice.
