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Adipocyte-derived chemerin rescues lipid overload-induced cardiac dysfunction
Ruimin Liu1,2, Yinying Han2, Chenglong Huang3
1Department of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing 400032, PR China.
Insights
Chemerin, a protein from fat cells, protects the heart in obesity. Lack of chemerin (Rarres2) worsens heart dysfunction and metabolic issues in mice on a high-fat diet.
Area of Science:
- Cardiovascular Biology
- Metabolic Syndrome Research
- Adipokine Signaling
Background:
- Chemerin, an adipocyte-secreted protein, is implicated in metabolic syndrome and cardiac function.
- Obesity and diabetes mellitus are associated with altered chemerin levels and cardiac health.
- The specific role of chemerin in high-fat diet-induced cardiac dysfunction requires further elucidation.
Purpose of the Study:
- To investigate the role of adipokine chemerin in high-fat diet-induced cardiac dysfunction.
- To determine the effects of chemerin deficiency on lipid metabolism, inflammation, and cardiac function.
- To explore the potential cardioprotective effects of chemerin in obesity-related cardiomyopathy.
Main Methods:
- Utilized chemerin (Rarres2) knockout mice fed normal or high-fat diets for 20 weeks.
- Assessed metabolic substrate flexibility, cardiac function, lipotoxicity, insulin resistance, and inflammation.
- Employed an in vitro model of lipid-overload cardiomyocytes to test chemerin supplementation.
Main Results:
- Rarres2 knockout mice on a normal diet exhibited normal metabolic and cardiac function.
- High-fat diet-fed Rarres2 knockout mice developed lipotoxicity, insulin resistance, inflammation, metabolic inflexibility, and cardiac dysfunction.
- In vitro, chemerin supplementation reversed lipid-induced abnormalities in cardiomyocytes.
Conclusions:
- Adipocyte-derived chemerin acts as an endogenous cardioprotective factor against obesity-related cardiomyopathy.
- Chemerin deficiency exacerbates metabolic substrate inflexibility and cardiac dysfunction under high-fat diet conditions.
- Targeting chemerin signaling may offer therapeutic potential for managing obesity-induced cardiac complications.
Abstract:
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.
