October 19, 2017

New study demonstrates how the gut bacteria causes obesity

According to a new study published in Nature, a research team from Yale has identified the mechanism in which gut dysbiosis leads to obesity. Previous research has demonstrated the association of the gut microbiome with metabolic markers and type II diabetes. Obesity is linked to changes in the gut bacteria, however, this mechanism was unclear.

In a previous study researchers discovered that one of the short chain fatty acids (SCFAs), acetate, stimulated the secretion of insulin in mice. When they compared acetate to other SCFAs, they discovered higher acetate levels in those that consumed a high fat diet. They also saw that acetate stimulated insulin secretion by beta cells in the pancreas, but this mechanism was not clear.

Interestingly, when acetate was then injected directly into the brain, it caused an increased release of insulin stimulating the parasympathetic nervous system. As a result, the increased acetate stimulates the beta cells of the pancreas to secrete more insulin in response to glucose. This also stimulates the secretion of gastrin and ghrelin causing an increase in food intake.

To establish a causal relationship between the gut microbiota and increased insulin, the research team transferred fecal matter from one group of mice to another. As a result, they observed similar changes in the gut microbiota with acetate levels and insulin.

In summary, this research demonstrates an association of alterations in the gut microbiota as a result of dietary changes leading to an increased acetate production. Furthermore, the increased acetate leads to increased food intake causing metabolic syndrome, insulin resistance, and obesity.

The research team suggests this mechanism may have played a role in evolution by stimulating animals to fatten up in times of food scarcity.

I was also a probiotic workshop at Yale last March and I remember one of the presentations from Max Nueuwdrop, MD, PHD, an internist and endocrinologist, from Amsterdam. He went into detail on the microbiota and metabolism. He showed how butyrate, a SCFA, improved insulin resistance and brown fat activation. In general, low short chain fatty acids (SCFAs) are associated with low diversity and abundance of the commensal bacteria. We typically want to see high levels of butyrate and not acetate. When patients introduce probotics and increase their dietary fiber intake by consuming fruits and vegetables, the beneficial bacteria butyrate, and SCFAs increase.

Probiotics help encourage microbial diversity, especially if the probiotic supplement is of mixed species. In ecological terms, it is more stable to have diverse populations in any ecosystem. The same is true for the gastrointestinal microbiome.

This also bring up the importance of stool testing in patients with metabolic syndrome and diabetes and just looking at facing glucose, insulin, A1c, and lipid profiles.

Other research has indicated that obesity has a microbial component that alters the caloric extraction from ingested food. For example, If you have more Bacteroidetes, the individual tends to be leaner. High Firmicutes:Bacteroidetes ratios have been known to increase the caloric extraction from food and these individuals tend to be more obese. This also ties together the importance of dietary fiber and weight loss.

By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS

Source: Rachel J. Perry, Liang Peng, Natasha A. Barry, Gary W. Cline, Dongyan Zhang, Rebecca L. Cardone, Kitt Falk Petersen, Richard G. Kibbey, Andrew L. Goodman, Gerald I. Shulman. Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome.Nature, 2016; 534 (7606): 213 DOI: 10.1038/nature18309

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