Abstract
Meta-analyses suggest that yogurt consumption reduces type 2 diabetes incidence in humans, but the molecular basis of these observations remains unknown. Here we show that dietary yogurt intake preserves whole-body glucose homeostasis and prevents hepatic insulin resistance and liver steatosis in a dietary mouse model of obesity-linked type 2 diabetes. Fecal microbiota transplantation studies reveal that these effects are partly linked to the gut microbiota. We further show that yogurt intake impacts the hepatic metabolome, notably maintaining the levels of branched chain hydroxy acids (BCHA) which correlate with improved metabolic parameters. These metabolites are generated upon milk fermentation and concentrated in yogurt. Remarkably, diet-induced obesity reduces plasma and tissue BCHA levels, and this is partly prevented by dietary yogurt intake. We further show that BCHA improve insulin action on glucose metabolism in liver and muscle cells, identifying BCHA as cell-autonomous metabolic regulators and potential mediators of yogurt’s health effects.
Highlights
Meta-analyses suggest that yogurt consumption reduces type 2 diabetes incidence in humans, but the molecular basis of these observations remains unknown
There is strong evidence from large prospective cohort studies and meta-analyses that yogurt consumption is associated with a lower type 2 diabetes (T2D) risk as compared to the total dairy intake, leading to the proposal that the health benefits may be linked to the fermentation process, the lactic acid bacteria (LAB), and/or host-microbial mechanisms that are induced during yogurt consumption[2,3,27]
We report that feeding yogurt corresponding to the equivalent of two servings per day, replacing 7.6% of the daily energy intake, prevents insulin resistance and hepatic steatosis in diet-induced obese mice
Summary
Meta-analyses suggest that yogurt consumption reduces type 2 diabetes incidence in humans, but the molecular basis of these observations remains unknown. The aim of this study was to determine the effect of yogurt intake on the development of whole-body and tissuespecific insulin resistance in a mouse model of obesity-linked T2D and to determine the potential role of the gut microbiota and hepatic metabolic pathways. We found that lyophilized yogurt intake (equivalent to two servings of yogurt) reduced the development of high-fat diet-induced insulin resistance, which was linked to its effects on liver metabolism and the gut microbiota. These beneficial metabolic effects of yogurt intake were associated with an increase of branched-chain hydroxy acids (BCHA) in the liver of these animals. Our work identifies BCHA as new milk fermentation-derived molecules that potentially contribute to the beneficial effects of yogurt intake on T2D and related metabolic disturbances
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