Reams of research have linked obesity, insulin resistance and metabolic syndrome with changes to gut microbiota.
New research from Yale reveals “a causal link between alterations in the gut microbiota in response to changes in the diet and increased acetate production.” In this rodent study, altered microbiota increased the production of acetate. The acetate stimulated the parasympathetic nervous system.
Acetate stimulates beta cells to secrete more insulin in response to glucose through a centrally mediated mechanism. It also stimulates secretion of the hormones gastrin and ghrelin, which lead to increased food intake.
The largest and most diverse colonies of microbiota reside in the large intestine and mouth.
An early hint that gut microbes might play a role in obesity came from studies comparing intestinal bacteria in obese and lean individuals. In studies of twins who were both lean or both obese, researchers found that the gut community in lean people was like a rain forest brimming with many species but that the community in obese people was less diverse—more like a nutrient-overloaded pond where relatively few species dominate.
Diet is an important factor in shaping the gut ecosystem. A diet of highly processed foods, for example, has been linked to a less diverse gut community in people. Gordon’s team demonstrated the complex interaction among food, microbes and body weight by feeding their humanized mice a specially prepared unhealthy chow that was high in fat and low in fruits, vegetables and fiber (as opposed to the usual high-fiber, low-fat mouse kibble). Given this “Western diet,” the mice with obese-type microbes proceeded to grow fat even when housed with lean cagemates. The unhealthy diet somehow prevented the virtuous bacteria from moving in and flourishing.
Obesity is a growing health issue in the U.S. Over the past 25 years, the obesity rate has almost doubled, nearly two-thirds of use are overweight, and 1-in-3 adults are clinically obese.