Bifidobacterium adolescentis attenuates cardiac remodeling in HFD/STZ-induced obesity-associated diabetic cardiomyopathy.

Obesity-associated diabetic cardiomyopathy is characterized by cardiac structural remodeling and modification of gene expression. Increasing evidence has led to the conclusion that gut microbiota, particularly probiotics, may modulate cardiac health through systemic and molecular pathways. The aim of the current study was to explore the cardioprotective effects of Bifidobacterium adolescentis on cardiac structure and gene expression in a rat model of high-fat diet (HFD) and low-dose streptozotocin (STZ)-induced obesity-associated diabetic cardiomyopathy. Male Wistar rats were divided into the following four groups: control, HFD, HFD- B. adolescentis (8 weeks), and HFD-B. adolescentis (16 weeks). Stereological studies were conducted to quantify left ventricular and myocardial volume. Real-time PCR was used to quantify the levels of genes associated with cardiac stress, fibrosis, inflammation, and contractility, like ANP, BNP, TGF-β, GATA4, Myc, Nfkb1, NPR1, Kcnq1, MEF2D, and SERCA2a. HFD/STZ treatment significantly increased heart weight (+ 68%) and left ventricular volume (+ 63%), elevated myocardial volume (+ 42%), and reduced vascular volume. Hypertrophic and inflammatory genes (ANP, BNP, TGF-β, GATA4, Myc, Nfkb1) were markedly upregulated, while contractility-related genes (MEF2D, SERCA2a, NPR1, KCNQ1) were downregulated. B. adolescentis supplementation for 8–16 weeks reversed these alterations, normalizing structural indices and restoring gene expression toward control levels. Bifidobacterium adolescentis attenuated obesity- and hyperglycemia-associated cardiac remodeling by improving structural and molecular parameters. These findings identify B. adolescentis as a potential probiotic candidate for preventing obesity-associated diabetic cardiomyopathy.