Fang Cheng, Xu Xiaomin, Lu Fang, Liu Shumin
Heilongjiang University of Chinese Medicine, Harbin, China.
Front Microbiol. 2025 Apr 8;16:1500935. doi: 10.3389/fmicb.2025.1500935. eCollection 2025.
The modification of gut microbiota has been linked to diabetic cardiomyopathy, yet the precise mechanisms through which gut microbes impact cardiac injury remain unclear. Our study concentrated on the gut microorganisms, the intestinal mucosal barrier, and the metabolic pathways involving glucose and lipids in mice afflicted with diabetic cardiomyopathy, while also investigating the cardioprotective properties of and . Using a db (Leptin receptor gene-deficient mouse) mouse model of diabetic cardiomyopathy, we observed that these mice exhibited a decline in the diversity of intestinal microbes, alterations in the abundance of diabetes-related microorganisms, a decrease in , an increase in , and an overall rise in intestinal microbial populations. We pinpointed the inflammatory response and the compromised permeability of the intestinal lining as key contributors to the decline of the intestinal mucosal barrier, subsequently leading to cardiac injury. Administering and was shown to restore the equilibrium of the intestinal microbiota, modify metabolic pathways involving glycerophospholipids, arachidonic acid, and additional metabolites within the myocardial tissue through bile acid, taurine, and associated metabolic processes, resulting in lessened cardiac dysfunction, hypertrophy, and fibrosis in the diabetic cardiomyopathy mice. In conclusion, our findings indicate that the intestinal microbiota, intestinal mucosal barrier, and glycolipid metabolism are disrupted in mice with diabetic cardiomyopathy; however, and may effectively reverse these alterations. These results offer valuable insights for creating therapeutic strategies aimed at mitigating cardiac damage linked to diabetes by focusing on the gut microbiota and glucose and lipid metabolism.
肠道微生物群的改变与糖尿病性心肌病有关，然而肠道微生物影响心脏损伤的确切机制仍不清楚。我们的研究集中在患有糖尿病性心肌病的小鼠的肠道微生物、肠道黏膜屏障以及涉及葡萄糖和脂质的代谢途径，同时还研究了[具体物质1]和[具体物质2]的心脏保护特性。使用糖尿病性心肌病的db（瘦素受体基因缺陷小鼠）小鼠模型，我们观察到这些小鼠肠道微生物的多样性下降、与糖尿病相关微生物的丰度改变、[物质1]减少、[物质2]增加以及肠道微生物总体数量上升。我们确定炎症反应和肠壁通透性受损是肠道黏膜屏障下降的关键因素，随后导致心脏损伤。结果表明，给予[具体物质1]和[具体物质2]可恢复肠道微生物群的平衡，通过胆汁酸、牛磺酸及相关代谢过程改变心肌组织中涉及甘油磷脂、花生四烯酸和其他代谢物的代谢途径，从而减轻糖尿病性心肌病小鼠的心脏功能障碍、肥大和纤维化。总之，我们的研究结果表明，糖尿病性心肌病小鼠的肠道微生物群、肠道黏膜屏障和糖脂代谢受到破坏；然而，[具体物质1]和[具体物质2]可能有效逆转这些改变。这些结果为制定旨在通过关注肠道微生物群以及葡萄糖和脂质代谢来减轻与糖尿病相关的心脏损伤的治疗策略提供了有价值的见解。
