 |
南京卡米洛生物工程有限公司
主營產(chǎn)品： 小鼠IgA類單克隆抗體腹水純化試劑盒,人17α-羥孕酮,豬雌二醇,白介素1受體拮抗劑 |
公司信息
恭喜南昌老師使用卡米洛(CAMILO)ELISA試劑盒發(fā)表文章
2024-3-19 閱讀(781)
| 文獻(xiàn)標(biāo)題 | Asprosin contributes to pathogenesis of obesity by adipocyte mitophagy induction to inhibit white adipose browning in mice | ||||
| 文獻(xiàn)作者 | Sheng Chen、Wanwan Yuan、Qianqian Huang、Xiaowei Xiong、Chaowen Wang、Wenjing Zeng、Li Wang、Yijun Huang、Yeyi Liu、Yan Wang、Qiren Huang | ||||
| 期刊名稱 | INTERNATIONAL JOURNAL OF OBESITY | 影響因子 | 4.9/Q2 | ||
| 發(fā)布時間 | 2024.02 | ||||
| 使用產(chǎn)品 | C57小鼠白脂素(Asprosin)ELISA試劑盒 | 貨號 | 2C57M-KMLJ221034 | ||
BACKGROUND: Asprosin (ASP) is a newly discovered adipokine secreted by white adipose tissue (WAT), which can regulate the homeostasis of glucose and lipid metabolism. However, it is not clear whether it can regulate the browning of WAT and mitophagy during the browning process. Accordingly, this study aims to investigate the effects and possible mechanisms of ASP on the browning of WAT and mitophagy in vivo and in vitro. METHODS: In in vivo experiments, some mouse models were used including adipose tissue ASP-specific deficiency (ASP–/– ), high fat diet (HFD)-induced obesity and white adipose browning; in in vitro experiments, some cell models were also established and used, including ASP-deficient 3T3-L1 preadipocyte (ASP–/– ) and CL-316243 (CL, 1 µM)-induced browning. Based on these models, the browning of WAT and mitophagy were evaluated by morphology, functionality and molecular markers. RESULTS: Our in vivo data show that adipose tissue-specific deletion of ASP contributes to weight loss in mice; supplementation of ASP inhibits the expressions of browning-related proteins including UCP1, PRDM16 and PGC1ɑ during the cold exposure-induced browning, and promotes the expressions of mitophagy-related proteins including PINK1 and Parkin under the conditions of whether normal diet (ND) or HFD. Similarly, our in vitro data also show that the deletion of ASP in 3T3-L1 cells significantly increases the expressions of the browning-related proteins and decreases the expressions of the mitophagy-related proteins. CONCLUSIONS: These data demonstrate that ASP deletion can facilitate the browning and inhibit mitophagy in WAT. The findings will lay an experimental foundation for the development of new drugs targeting ASP and the clinical treatment of metabolic diseases related to obesity.
