CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD+-Sirt1-PGC1α signaling pathway
CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD+-Sirt1-PGC1α signaling pathway
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DOI：
10.1139/cjpp-2022-0454
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Lingfang Wang
中科院分区：
文献类型：
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作者：
Qi Ding;Ke Wen;Qian Li;Qi-Hang Zhao;Jia-Le Zhao;Yun-Fei Xiao;Xiao-Hui Guan;Mei-Xiu Jiang;Feng Zhang;Lingfang Wang
Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD induced obesity remain unknown. In this study, we established obesity model with HFD and examined the changes in metabolites with metabonomics. Our results showed that CD38 expression was increased in muscle and brown fat after HFD treatment. Moreover, the results of metabonomics showed that CD38 deficiency significantly altered the metabolites in energy metabolism, cofactor generation and redox homeostasis. Furthermore, CD38 deficiency reduced the expressions of NOX2 and FASN in mRNA level. We found the expressions of Sirt1, Sirt3 and PGC1α were up-regulated in CD38 deficient muscle tissue. In brown fat, the Sirt1-3, Cidea, ELOVL3 and Dio2 expressions were increased in CD38 deficiency mice. Our results showed the UCP1 expression was up-regulated. And supplement NAD+ increased the expression of Sirt1 and PGC1α after palmitic acid treatment. Taken together, our results demonstrated that the protection of CD38 deficiency on HFD-induced obesity was related to inhibition oxidative stress and increasing energy expenditure via activating NAD+/Sirtuins signaling pathways in muscle and brown fat.
