Comments on “Probiotic Bifidobacterium strains and galactooligosaccharides improve intestinal barrier function in obese adults but show no synergism when used together as synbiotics”

Abstract

The development of obesity is influenced by various factors; however, in recent decades, researchers have been particularly intrigued by the role of gut microbiota. Specific changes in bacterial taxa and a decrease in diversity within the gut microbiota are observed among obese individuals (Hou et al., 2017). These changes contribute to an elevation in intestinal permeability and translocation of lipopolysaccharide (LPS) into blood circulation, leading to metabolic endotoxemia (Mohammad and Thiemermann, 2021). LPS has been proven to increase tight junction permeability by inducing enterocyte membrane expression and localization of Toll-like Receptor-4 (Guo et al., 2013). Obesity has been linked to elevated intestinal permeability. In genetically obese mice, there is an upregulation of intestinal permeability along with an increase in circulating endotoxins and pro-inflammatory cytokines such as interleukin one beta (IL-1β), interleukin-6 (IL-6), interferon-gamma (INFγ), and tumor necrosis factor (TNF-α), when compared to wild-type mice (Lee et al., 2018). Conversely, obesity induced by a high-fat diet, also known as diet-induced obesity (DIO), is associated with alterations in the gut microbial population that are associated with inflammation and heightened intestinal permeability, likely due to diminished expression of tight junction (TJ)-related genes, including ZO-1 and occludin.