Key result
Chemerin reverses lipotoxicity-induced cardiac dysfunction and insulin resistance in Rarres2-deficient mice.
Why the study?
The roles of adipokine chemerin in high fat-induced cardiac dysfunction and its effects on lipid metabolism, inflammation, and cardiac function were not fully understood.
Chemerin loss worsens high-fat diet cardiac dysfunction in mice; leaves open its cardioprotective role in human obesity cardiomyopathy.
Chemerin, an adipocyte-secreted protein, has been recently suggested to be linked to metabolic syndrome and cardiac function in obese and diabetes mellitus. This study aimed to investigate the potential roles of adipokine chemerin on high fat-induced cardiac dysfunction. Chemerin ( Rarres2 ) knockout mice, which were fed with either a normal diet or a high-fat diet for 20 weeks, were employed to observe whether adipokine chemerin affected lipid metabolism, inflammation, and cardiac function. Firstly, we found normal metabolic substrate inflexibility and cardiac function in Rarres2 −/− mice with a normal diet. Notably, in a high-fat diet, Rarres2 −/− mice showed lipotoxicity, insulin resistance, and inflammation, thus causing metabolic substrate inflexibility and cardiac dysfunction. Furthermore, by using in vitro model of lipid-overload cardiomyocytes, we found chemerin supplementation reversed the lipid-induced abnormalities above. Herein, in the presence of obesity, adipocyte-derived chemerin might function as an endogenous cardioprotective factor against obese-related cardiomyopathy.
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Liu et al. (2023) studied High fat-induced cardiac dysfunction. Chemerin (Rarres2) knockout and chemerin supplementation vs. Normal diet / unsupplemented lipid-overload cardiomyocytes was evaluated on Lipid metabolism, inflammation, and cardiac function. In a high-fat diet, Rarres2 knockout mice developed lipotoxicity, insulin resistance, and cardiac dysfunction, which were reversed by chemerin supplementation in vitro.
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