Probiotic Lactobacillus reuteri KUB-AC5 provides cardioprotection via mitigating cardiac mitochondrial dysfunction in obese rats.

Cardiac mitochondrial dysfunction is a crucial mechanism underlying obesity-induced cardiovascular diseases. A close link between obesity and gut microbiota has been revealed, and the benefits of gut microbiota modulation by probiotics have been widely identified. Although the probiotic Lactobacillus reuteri KUB-AC5 exerted anti-inflammatory activity and enhanced the activity of beneficial microbes, the effects of this probiotic on mitochondria in the obese heart have never been investigated. Male Wistar rats were divided into four groups to receive either a normal diet (ND; n = 9) or a high-fat and high-calorie diet (HFCD; n = 30) for 24 weeks. At the beginning of week 13, ND-fed rats received vehicle, while HFCD-fed rats were further subdivided into three groups (n = 10/group) to receive either vehicle, a live probiotic Lactobacillus reuteri KUB-AC5, or a heat-killed probiotic Lactobacillus reuteri KUB-AC5. At the end of week 24, cardiac functions were evaluated. The rats were then euthanized to enable blood and cardiac ventricle collection. Evidence from the obese rats treated with Lactobacillus reuteri KUB-AC5 in both forms indicated reduced body weight and attenuated insulin resistance. Regarding the heart, obese rats treated with either form of Lactobacillus reuteri KUB-AC5 had improved cardiac functions, mitochondrial dynamics, mitochondrial biogenesis, fat and ketone body utilization, anaplerosis, ATP production, and oxidative phosphorylation. In addition, treatment with this probiotic diminished oxidative stress and restored the antioxidative capacity of cardiac mitochondria. Our preclinical findings in male rats highlighted the benefits of the probiotic Lactobacillus reuteri KUB-AC5, given in both live and heat-killed forms, in alleviating obesity-induced cardiac mitochondrial dysfunction.