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Health benefits of yogurt consumption in obese mice

ABSTRACT: The gut microbiota and fermentation-derived branched chain hydroxy acids mediate the health benefits of yogurt consumption in obese mice

PROVIDER: PRJEB47834 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6876550.fastq.gz	Fastqsanger.gz
	ERR6876560.fastq.gz	Fastqsanger.gz
	ERR6876570.fastq.gz	Fastqsanger.gz
	ERR6876580.fastq.gz	Fastqsanger.gz
	ERR6876590.fastq.gz	Fastqsanger.gz

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Gut microbiota and fermentation-derived branched chain hydroxy acids mediate health benefits of yogurt consumption in obese mice

Project description: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.

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Project description:Modern lifestyle is associated with a major consumption of ultra-processed foods (UPF) due to their practicality and palatability. The ingestion of emulsifiers, a main additive in UPFs, has been related to gut inflammation, microbiota dysbiosis, adiposity and obesity. Maternal unbalanced nutritional habits during embryonic and perinatal stages perturb offspring’s long-term metabolic health, thus increasing obesity and associated comorbidity risk. However, whether maternal emulsifier consumption influences developmental programming in the offspring remains unknown. Here we show that, in mice, maternal consumption of dietary emulsifiers (1% CMC and 1% P80 in drinking water), during gestation and lactation, perturbs the development of hypothalamic energy balance regulation centers of the progeny, leads to metabolic impairments, cognition deficits and induces anxiety-like traits in a sex-specific manner. Our findings support the notion that maternal consumption of emulsifiers, common additives of UPFs, causes mild metabolic and neuropsychological malprogramming in the progeny. Our data call for nutritional advice during gestation.

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