Gut microbiota might mediate the benefits of high-fiber/acetate diet to cardiac hypertrophy mice

• Chen, Meifang ^[1] ; Peng, Liming ^[2] ; Zhang, Chenglong ^[3] ; Liu, Qiong ^[3] ; Long, Tianyi ^[3] ; Xie, Qiying ^[3]
  1. [1] Department of Geriatric Cardiology, Xiangya Hospital, Central South University, Changsha 41008, China ; Department of Cardiology, Xiangya Hospital, Central South University, #87 Xiangya Road, Kaifu District, Changsha 410008, Hunan, China
  2. [2] Department of Cardiology, Xiangya Hospital, Central South University, #87 Xiangya Road, Kaifu District, Changsha 410008, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, China; Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, China
  3. [3] Department of Cardiology, Xiangya Hospital, Central South University, #87 Xiangya Road, Kaifu District, Changsha 410008, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, China

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• Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 79, Nº. 4, 2023, págs. 745-756
• Idioma: inglés
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• Resumen

  • Continuously prolonged cardiac hypertrophy results in maladaptive myocardial remodeling, which afects cardiac function and can eventually lead to heart failure. Short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, have been reported to be associated with cardiovascular diseases (CVD). Gut microbiota may mediate between dietary fber and SCFA efects on cardiac hypertrophy. The mice model of isoproterenol (ISO)-induced cardiac hypertrophy was constructed and verifed for physiological, functional, and fbrotic alterations in this study. Both high-fber and acetate diet improved physiological indexes, ameliorated cardiac functions, and relieved fbrotic alterations in model mice hearts; collectively, cardiac hypertrophy in mice receiving both high-fber and acetate diet improved. Following 16s rDNA sequencing and integrative bioinformatics, analyses indicated that both high-fber and acetate diet caused alterations in mice gut microbiota compared with the ISO group, including OTU composition and abundance. In conclusion, high-fber and acetate diet improve the physiological status, cardiac functions, and fbrotic alterations in ISO-induced hypertrophic mice. Besides, considering the alterations in mice gut microbiota in response to single ISO, both high-fber and acetate diet treatment, gut microbiota might mediate the favorable benefts of both high-fber and acetate diet on cardiac hypertrophy.