脂联素
内分泌学
内科学
雷公藤醇
瘦素
胰岛素抵抗
肥胖
代谢综合征
基因剔除小鼠
化学
医学
细胞凋亡
受体
生物化学
作者
Ling Ye,Yan Gao,Xuecheng Li,Xiaoshuang Liang,Yi Yang,Rufeng Zhang
标识
DOI:10.1080/13813455.2023.2250929
摘要
AbstractBackgound: Celastrol, a leptin sensitiser, has been shown to inhibit food intake and reduce body weight in diet-induced obese mice, making it a potential treatment for obesity and metabolic diseases. Adiponectin signalling has been reported to play an important role in the treatment of obesity, inflammation, and non-alcoholic fatty liver disease.Materials and methods: Wild-type (WT) and AdipoR1 knockout (AdipoR1-/-) mice were placed on a chow diet or a high-fat diet (HFD) and several metabolic parameters were measured. Celastrol was then administered to the HFD-induced mice and the response of WT and AdipoR1-/- mice to celastrol in terms of body weight, blood glucose, and food intake was also recorded.Results: AdipoR1 knockout caused elevated blood glucose and lipids, impaired glucose tolerance and insulin resistance in mice, as well as increased susceptibility to HFD-induced obesity. After 14 days of treatment, WT and AdipoR1-/- mice showed significant reductions in body weight and blood glucose and improvements in glucose tolerance.Conclusion: The present study demonstrated that AdipoR1 plays a critical role in metabolic regulation and that the improvement of weight and metabolic function by celastrol is independent of the AdipoR1-mediated signalling pathway.Keywords: AdipoR1celastrolobesityNAFLD Disclosure statementNo potential conflict of interest was reported by the author(s).Data availability statementThe authors confirm that the data supporting the findings of this study are available within the article or its supplementary materials.Additional informationFundingThis study was supported by the Biocytogen Pharmaceuticals (Beijing) Co., Ltd.
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