ArticleFrontiers in endocrinology2021
Proteomic and Structural Manifestations of Cardiomyopathy in Rat Models of Obesity and Weight Loss.
Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- Immunometabolic Dysregulation in Obesity: Integrating Macrophage Polarization, Metabolic Reprogramming, and Gut Microbiota Crosstalk.Immunity, inflammation and disease · 2026Review
- Review
- Effects of High-Fat Diet on Cardiovascular Protein Expression in Mice Based on Proteomics.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Effect of high-fat diet and empagliflozin on cardiac proteins in mice.Nutrition & metabolism · 2022Article
- UTP14A, DKC1, DDX10, PinX1, and ESF1 Modulate Cardiac Angiogenesis Leading to Obesity-Induced Cardiac Injury.Journal of diabetes research · 2022Article
- Effects of Semaglutide on Cardiac Protein Expression and Cardiac Function of Obese Mice.Journal of inflammation research · 2022Article
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Authors and funding
6 authors at 3 institutions in 1 country.
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Abstract
Obesity cardiomyopathy increases the risk of heart failure and death. Obesity is curable, leading to the restoration of the heart phenotype, but it is not clear if there are any after-effects of obesity present after weight loss. We characterize the proteomic landscape of obesity cardiomyopathy with an evaluation of whether the cardiac phenotype is still shaped after weight loss. Cardiomyopathy was validated by cardiac hypertrophy, fibrosis, oversized myocytes, and mTOR upregulation in a rat model of cafeteria diet-induced developmental obesity. By global proteomic techniques (LC-MS/MS) a plethora of molecular changes was observed in the heart and circulation of obese animals, suggesting abnormal utilization of metabolic substrates. This was confirmed by increased levels of cardiac ACSL-1, a key enzyme for fatty acid degradation and decreased GLUT-1, a glucose transporter in obese rats. Calorie restriction and weight loss led to the normalization of the heart's size, but fibrosis was still excessive. The proteomic compositions of cardiac tissue and plasma were different after weight loss as compared to control. In addition to morphological consequences, obesity cardiomyopathy involves many proteomic changes. Weight loss provides for a partial repair of the heart's architecture, but the trace of fibrotic deposition and proteomic alterations may occur.
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