Abstract
Intermittent fasting (IF) plays an essential role in improving lipid metabolism disorders caused by metabolic cardiomyopathy. Growing evidence revealed that N6-methyladenosine (m6A) RNA methylation is related to obesity and lipid metabolic. Our study aimed to assess the beneficial effects of IF on lipid deposition, apoptosis, and m6A methylation in high-fat diet (HFD)-induced obesity cardiomyopathy. Male C57BL/6J mice were fed a normal diet (ND) or HFD ad libitum for 13 weeks, after which time a subgroup of HFD mice were subjected to IF for 24 h and fed HFD in the other day for 8 weeks. We found that IF intervention significantly improved cardiac functional and structural impairment and serum lipid metabolic disorder induced by HFD. Furthermore, IF intervention decreased the mRNA levels of the fatty acid uptake genes of FABP1, FATP1, and CD36 and the fatty acid synthesis genes of SREBF1, FAS, and ACCα and increased the mRNA levels of the fatty acid catabolism genes of ATGL, HSL, LAL, and LPL in cardiac tissueof HFD-induced obese mice. TUNEL-positive cells, Bax/Bcl-2 ratio, and Cleaved Caspase-3 protein expression in HFD-induced obese mice hearts was down-regulated by IF intervention. In addition, IF intervention decreased the m6A methylation levels and METTL3 expression and increased FTO expression in HFD-induced obesity cardiomyopathy. In conclusion, our findings demonstrate that IF attenuated cardiac lipid deposition and apoptosis, as well as improved cardiac functional and structural impairment in HFD-induced obesity cardiomyopathy, by a mechanism associated with decreased m6A RNA methylation levels.
Highlights
Publisher’s Note: MDPI stays neutralObesity cardiomyopathy is defined as obesity-induced impairment in the cardiac architecture and function that is independent of hypertension, coronary heart disease, and other heart diseases [1,2]
Echocardiography was performed in High-fat diet (HFD) mice to determine whether Intermittent fasting (IF) had an improvement effect on cardiac function
hematoxylin and eosin (H&E) and Masson staining indicated that morphological abnormalities and interstitial fibrosis were observed in the myocardial tissues of obese mice; the above damage was remarkably reversed in HFD-IF groups (Figure 2J–L)
Summary
Publisher’s Note: MDPI stays neutralObesity cardiomyopathy is defined as obesity-induced impairment in the cardiac architecture and function that is independent of hypertension, coronary heart disease, and other heart diseases [1,2]. High-fat diet (HFD)-induced obesity cardiomyopathy is characterized by abnormal heart structure and dysfunction, such as echocardiographic changes consistent with poor systolic function, enhanced cardiac lipid deposition, and apoptosis [3,4,5]. Intermittent fasting (IF), a nutritional approach in which ad libitum feeding is alternated with fasting periods, has been shown to have cardioprotective effects in the heart [9,10]. Both clinical and experimental evidence has revealed that IF extends lifespan, decreases myocardial with regard to jurisdictional claims in published maps and institutional affiliations
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