High Levels of Akkermansia muciniphilia Growth Associated With Spring Water Ingestion Prevents Obesity and Hyperglycemia in a High-fat Diet-Induced Mouse Model

Abstract

Background: Type 2 diabetes may be alleviated by mineral water (MW) ingestion. We investigated whether spring water (SW) (a kind of mixed MW) ingestion influences metabolic parameters via alteration of the gut microbiota in high-fat diet (HFD)-fed mice. Method: We divided 32 C57/BL mice into 4 equal groups: normal diet with tap water (Control), high-fat diet with tap water (HFD), normal diet with SW (SW), and high-fat diet with SW (HFD + SW). During this experiment, we checked the body weight (BW) with fasting blood sugar (FBS) every week and all mice were sacrificed in the 17th week to observe serological markers, internal organs, and composition of gut microbiota. Results: The BW of HFD-fed mice was significantly higher than that of mice fed an HFD + SW diet in the early period of the experiment. Fasting blood glucose (FBG) in the HFD group showed a fluctuating pattern compared to the HFD + SW group, and the area under the curve (AUC) value of the oral glucose tolerance test (OGTT) was significantly greater in the HFD group than in the HFD + SW group. Serologic markers were not significantly different between the HFD and HFD + SW groups. Histologically, the most severe fatty changes in the liver were observed in the HFD group. Lastly, the gut levels of Akkermansia muciniphilia were 100-fold higher in the HFD + SW group than in the HFD mice. Conclusion: These findings indicate that SW ingestion, and the associated high levels of A muciniphilia growth in the gut, may improve the early stage of obesity and ameliorate HFD-induced hyperglycemia.

Dendrobium officinale polysaccharide attenuates type 2 diabetes in mice model by modulating gut microbiota and alleviating intestinal mucosal barrier damage

“…When intestinal permeability increases, excessive endotoxin can enter the blood circulation and trigger inflammation cascade reaction and disrupt homeostasis of intestinal barrier function [16] . Recent studies have confirmed that increased intestinal permeability and intestinal-derived LPS translocation are important causes of metabolic inflammation in T2DM [17][18] . Therefore, targeting intestinal barrier is a promising strategy for the treatment of T2DM.…”