Inflammation in visceral adipose tissues (VATs) contributes to the pathology of diabetes. This study focused on the inflammatory regulation in VATs by a yeast β-1,3-glucan (BYG) orally administered to ob/ob mice. BYG decreased pro-inflammatory modulators of TNF-α, IL-6, IL-1β, CCL2, and SAA3, and increased anti-inflammatory factors of Azgp1 (2.53 ± 0.02-fold change) at protein and/or mRNA levels (p < 0.05). Remarkably, BYG decreased the degree of adipose tissue macrophages (ATMs) infiltration to 82.5 ± 8.3%, especially the newly recruited ATMs. Interestingly, BYG increased the protective Th2 cell regulator GATA3 (7.72 ± 0.04-fold change) and decreased immunosuppressors IL-10 and IL-1ra, suggesting that BYG elicited inflammation inhibition via stimulating immune responses. Additionally, BYG increased the gut microbiota proportion of Akkermansia from 0.07% to 4.85% and improved the microenvironment of VATs through decreasing fibrosis and angiogenesis. These findings suggest that BYG has anti-inflammatory effect in diabetic mice, which can be used as a food component and/or therapeutic agent for diabetes.
Keywords: adipose tissue; gut microbiota; inflammation; obesity; yeast β-glucan.