The Potential of Probiotics in Preventing Diet-Induced Mitochondrial Dysfunction
According to the oxidative stress theory, reactive species are key drivers of inflammation and cardiovascular disease (1). The electron transport chain of the mitochondria accounts for ≈90 of the intracellular radioactive oxygen species (2). Interestingly, while low-carbohydrate high-protein diets promote weight loss, animal experiments show that they could also lead to mitochondrial dysfunction and therefore, oxidative stress and inflammation (3). In parallel, research in the last decade has unravelled the role of the healthy gut microbiome in preventing diseases, and probiotic supplements that alter the gut's composition show promise as a nutraceutical intervention to improve systemic low-grade inflammation, oxidative stress, body weight as well as insulin resistance and blood lipids (4,5). The objective of the study was to evaluate the potential of anti-inflammatory probiotics (B. Bifidum Rossel-71 and L. Helveticus) in preventing mitochondrial dysfunction. Apolipoprotein-E knockout mice were placed in 3 diet groups including a control, western type (high fat and carbohydrates), and low-carbohydrate high-protein diet. Each group was then further divided in 3 subgroups based on the dose of probiotics administered, including a control, low (0.5 B/does) and high (5 B/dose) dose of probiotics, for a total of 9 groups. Mitochondrial respiration data will be shown for 4-8 animals/group from our ongoing study. The animals' body weight and water consumption were monitored weekly. After 6 weeks, the liver's mitochondrial function was analyzed in depth using a sequential substrate addition protocol. This project will contribute to our understanding of the potential of probiotics in preventing oxidative stress, which could have immense economic and clinical implications.