After several hints that gut microbes may be key players in the obesity epidemic, a new study provides a mechanistic explanation of how the intestinal inhabitants directly induce hunger, insulin resistance, and ultimately obesity in rodents.
After mice and rats were fed a high-fat diet, their gut microbes produced more acetate, a short-chain fatty acid made during bacterial fermentation.
That acetate spread throughout the rodents bodies and into their brains where it activated the parasympathetic nervous system.
By activating the parasympathetic nervous system, the microbe-made acetate spurred the rodents to produce more insulin, a hormone made by pancreatic β-cells that promotes calorie storage, as well as ghrelin, a hormone involved in hunger.
The result was rodents that ate more developed insulin resistance—a precursor to diabetes—and became obese, the researchers report in Nature.
This generates a positive feedback loop, the authors conclude—which makes sense for foraging animals, they add.