Yogurt supplementation attenuates insulin resistance in obese mice by reducing metabolic endotoxemia and inflammation

Background

Inflammation is an underlying mechanism for development of obesity-related health complications. Yogurt consumption inhibits obesity-associated inflammation, but the tissue-specific mechanisms have not been adequately described.

Objectives

We aimed to determine the tissue-specific responses by which yogurt supplementation inhibits inflammation.

Methods

C57BL/6 male mice (5 weeks old) were fed a Teklad Global 14% Protein Rodent Maintenance diet as a control or a high-fat diet (60% calories from fat) to induce obesity for 11 weeks, followed by feeding a Western diet (WD; 43% carbohydrate & 42% fat) or WD supplemented with 5.6 % lyophilized yogurt powder for 3 weeks to test for the impact of yogurt supplementation. Markers of metabolic endotoxemia and inflammation were assessed in plasma and tissues. Cecal and fecal microbiota were profiled by 16S rRNA sequencing.

Results

In obese mice, relative to the WD control group, yogurt supplementation attenuated HOMA-IR by 57%) (p=0.020), plasma TNF-a by 31% (p<0.05) and colonic IFN-g by 46% (p=0.0034), which were accompanied by a 40% reduction in plasma LBP (p=0.0019) and 45% less colonic Lbp expression (p=0.037), as well as alteration in the beta diversity of cecal microbiota (p=0.0090) and relative abundance of certain cecal microbes (e.g., Lachnospiraceae Dorea longicatena with p=0.049). There were no differences in the LBP, Lbp, and Cd14 levels in the liver and small intestine between obese mice with and without yogurt supplementation (p>0.05).

Conclusions

Yogurt consumption inhibited obesity-induced inflammation in mice by modulating colonic endotoxin detoxification, changing the gut microbiota, and improving glucose metabolism. This work helps to establish the underlying mechanisms by which yogurt consumption affects markers of metabolic and immune health.