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In recent years, many studies have been dedicated towards elucidating the role of the intestinal microbiota in metabolic health. It was suggested that specific intestinal microbial compositions can either protect from—or contribute to obesity and metabolic diseases. A causal relation between the microbiota and host metabolic profile was demonstrated when faecal microbiota of lean and obese subjects was transferred into mice, which then exhibited corresponding phenotypes.1 Short chain fatty acids (SCFAs) have broadly been proposed as key mediators in the microbiota-induced metabolic effects on the host. They are produced by bacterial fermentation of otherwise indigestible nutrients. The most abundant SCFAs are propionate, acetate and butyrate. All have been extensively studied in murine models for their possible influence on colonic health, glucose and lipid metabolism, as well as appetite and energy expenditure. Although various mechanisms by which these SCFAs exert their effect were suggested,2–7 the precise pathways remain unclear.
In Gut, Li et al report on the mechanisms by which butyrate positively influences energy balance and protects from diet-induced obesity. They deduce that many of the butyrate-induced metabolic benefits are driven by a decrease in energy intake. In their first experiment, Li et al exposed overnight fasted mice to either intravenously administered butyrate or to butyrate administered via intragastric gavage. Interestingly, only intragastric administration affected feeding behaviour, reducing cumulative 24 hours food intake by 21%. Furthermore, it induced a marked shift in the activity of hypothalamic orexigenic and anorexic neurons. This demonstrates that butyrate administration affects central appetite regulation before butyrate enters …
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