Microbiota and obesity

Positive Feedback loop

Sergey Syrov, XXII CENTURY, based on the materials of Yale University: Study reveals how altered gut microbes cause obesity

Obesity is associated with changes in our microbiota – the community of microbes in the gut, the trillions of tiny organisms that inhabit us. But the mechanism of this process is not fully understood. In a new study published in the journal Nature (Perry et al., Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome), scientists from Yale University studied how altered intestinal microflora leads to obesity.

In an early study, Gerald I. Shulman, MD, a professor at Yale University, noted that acetate (the salt of acetic acid) stimulates insulin secretion in rodents. To learn more about the role of acetate, Shulman and a team of researchers from Yale conducted a series of experiments on animal models of obesity.

The research team measured levels of acetate and derivatives of other short-chain fatty acids and found higher levels of acetate in animals that consumed high-fat foods. It has also been observed that the administration of acetate stimulates the secretion of insulin by beta cells in the pancreas, although it is unclear how.

Further, the researchers determined that if acetate was injected directly into the brain, increased insulin production begins, caused by activation of the parasympathetic nervous system. "Acetate stimulates beta cells to secrete more insulin in response to glucose through a mechanism whose connecting link is the central nervous system," says Shulman. "It also stimulates the secretion of the hormones gastrin and ghrelin, which contribute to increased food intake."

Finally, the research team established a causal relationship between the gut microbiota and elevated insulin levels. After transferring the fecal masses of rodents of one group to rodents of another, the latter have similar changes in the intestinal microbiota – the level of acetate and insulin increases.

"All together, these experiments demonstrate a causal relationship between changes in the gut microbiota in response to dietary changes and an increase in acetate production," Shulman concludes. "An increase in the level of acetate, in turn, leads to an increase in food intake, a positive feedback is activated, which leads to obesity and insulin resistance," he explained.

Interestingly, in a recent study, experts from Imperial College London showed that the presence of acetate in the intestine and the ingestion of a small amount of acetic acid in the brain reduced appetite in mice. However, with a diet with a high content of fiber, not fat. So, perhaps, the cause of obesity is not the acetates themselves, but their source – VM.

The authors of the study suggest that this positive feedback loop may have played an important role in evolution, encouraging animals to eat a lot when they were faced with an excess of high-calorie food in a general food shortage situation.

"Changes in the intestinal microflora are associated with obesity and metabolic syndrome in humans as well as in rodents,– Shulman noted. "In this study, we propose a new explanation for this biological phenomenon in rodents, and we are now studying whether this mechanism works in humans."

Portal "Eternal youth" http://vechnayamolodost.ru  17.06.2016