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• W4207034916 abstract "Obesity has become a serious global public health problem, and cardiomyopathy caused by obesity has recently gained attention. As an important protein involved in glucose and lipid metabolism, G protein-coupled receptor 40 (GPR40) exerts cardioprotective effects in some disease models. This study aimed to explore whether GPR40 plays a protective role in obesity-induced cardiomyopathy. We established an obesity model by feeding rats with a high-fat diet, and H9c2 cells were stimulated with palmitic acid to mimic high fat stimulation. Overexpression of GPR40 was achieved by infection with lentivirus or cDNA plasmids. Obesity-induced cardiac injury models exhibit cardiac dysfunction, myocardial hypertrophy, and collagen accumulation, which are accompanied by increased inflammation, oxidative stress, and apoptosis. However, GPR40 overexpression attenuated these alterations. The anti-inflammatory effect of GPR40 may be by inhibiting the nuclear factor-κB pathway, and the antioxidative stress may occur as a result of nuclear transcription factor erythroid 2-related factor 2 pathway activation. In terms of the mechanisms of GPR40 against obese cardiomyopathy, GPR40 overexpression not only activated the sirtuin 1 (SIRT1)-liver kinase B1 (LKB1)-AMP-activated protein kinase (AMPK) pathway but also enhanced the binding of SIRT1 to LKB1. The antifibrotic, anti-inflammatory, antioxidative stress, and antiapoptotic effects of GPR40 overexpression were inhibited by SIRT1 small interfering RNA. In conclusion, GPR40 overexpression protects against obesity-induced cardiac injury in rats, possibly through the SIRT1-LKB1-AMPK pathway." @default.
• W4207034916 created "2022-01-26" @default.
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• W4207034916 date "2022-06-01" @default.
• W4207034916 modified "2023-10-02" @default.
• W4207034916 title "Overexpression of G Protein-Coupled Receptor 40 Protects Obesity-Induced Cardiomyopathy Through the SIRT1/LKB1/AMPK Pathway" @default.
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• W4207034916 doi "https://doi.org/10.1089/hum.2021.176" @default.
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