(P06-124-20) Anthocyanin Improves Glucose Homeostasis in Obese Mice via Regulation of Intestinal Microbiota and Barrier Function

Objectives: Anthocyanin (ACN) with low bioavailability possess anti-diabetic effect, the mechanism of the action remained unclear. This study aimed to investigate whether the anti-diabetic effects of anthocyanin were related to regulation of gut microbiota and epithelial barrier function.

Methods: Male C57Bl/6N mice were randomly assigned into 3 groups and fed chow, high fat/high sugar diet (HFHS, 45 kcal% fat, 17 kcal% sucrose) or HFHS + 0.4% anthocyanin for 8 weeks. Furthermore, a separate cohort of HFHS-fed C57Bl/6N mice were oral gavage with fecal microbiota from HFHS, HFHS+ACN and heat-killed fecal microbial from HFHS+ACN-fed donors (HK-ACN) for 4 weeks, The composition of gut microbiota, systemic inflammation, glucose homeostasis and intestinal barrier function were determined.

Results: The area under the curve (AUC) of the oral glucose tolerance test (GTT) and insulin tolerance test (ITT) in HFHS-fed mice were 61% and 79% higher than those in Chow-fed mice (P<0.05). ACN supplementation improved HFHS-induced glucose intolerance in the GTT (P<0.05) and restore insulin sensitivity in the ITT (P<0.05). ACN supplementation also attenuated HFHS-induced systemic inflammation, intestinal permeability and metabolic endotoxemia (P<0.05). In addition, ACN administration increased expression of epithelial barrier function genes ZO-1, Occludin and decreased inducible NO-synthase (iNOS) protein levels in intestine of HFHS-fed mice. Gut microbiota analysis showed that ACN greatly altered gut microbiota of HFHS-fed mice. Transplantation of the gut microbiota from ACN-fed mice, but not HFHS-fed or HK-ACN-fed mice, significantly improved intestinal epithelial barrier function, systemic inflammation and glucose homeostasis.

Conclusions: The present study demonstrated that ACN improves HFHS-induced impairment of glucose metabolism by regulating the gut microbiota and epithelial barrier functions.

Funding Sources: No funding sources to report