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Allele Deficiency of CTRP6 Affects the Browning of White Adipose Tissue in Mice
Kong Weili1#, Huang Xin1,2#, Xu Ke1,2, Ji Miao1,2, Li Yuan1, Lu Hailun1, Li Shihui1, Wu Wenjing1*, Zhang Jin1*
1College of Biological Chemical Sciences and Engineering, Jiaxing University, Jiaxing 314000, China; 2College of Agronomy and Biotechnology, Hebei Normal University of Science & Technology, Qinhuangdao 066000, China
Abstract: The C1q/TNF-related protein 6 (CTRP6) is an adipokine， which plays an important role in lipids metabolism of animals. Previously we reported that knockdown of CTRP6 via intraperitoneal injection of the CTRP6-shRNA lentivirus protected mice from diet-induced obesity. This study aimed to confirm the involvement of CTRP6 in body weight and browning of white adipose tissue with CTRP6+/– mice (KO mice) under cold exposure. In KO mice， CTRP6 mRNA expression was significantly downregulated to the level of that of wild type mice (WT mice). Then 4-week old male KO mice were randomly divided into two groups (5 mice/group)， cold exposure group (4 oC) and room temperature group (25 oC). The body weight and fat weight of mice were measured after the cold stimulation for 6 weeks. Compared with WT mice， the body weight and white fat weight of KO mice decreased significantly in both cold exposure group and room temperature group， whereas the weight of brown fat increased significantly. Additionally， the brown fat markers， such as UCP1， PRDM16 and PGC1α were found to be upregulated in the white and brown adipose tissue of the WT mice. Mechanistically， CTRP6 knockout also upregulated expression of mitochondrial metabolic factors NRF1， TFAM and Cyt c. The results suggested that CTRP6 knockout could inhibit white adipose tissue accumulation and promote browning of white adipose tissue. Therefore， this research established foundation to reveal CTRP6 physiological functions， which provides a theoretical reference for the treatment of human obesity and related metabolic diseases.
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