The microbiome and obesity

February 18, 2019

For more than a decade, scientists suspected that gut bacteria played a significant role in obesity.  Recent research by Dr. Gerald Shulman and colleagues sheds some light on the connection to obesity and possible therapeutic interventions!

The connection involves gut bacteria, the gut-brain axis, the parasympathetic nervous system, the pancreas, insulin, and metabolic changes.  The current hypothesis is that bacteria in the intestine produce acetate by fermentation.  Acetate is a short-chain fatty acid that triggers other metabolic signals and communicates with the brain through the gut-brain axis.  The brain then sends signals through the parasympathetic nervous system to the pancreas to produce more insulin and other compounds, which increase a person’s predisposition to gain weight.

This hypothesis is well supported by scientific evidence.  When animals were given food rich in fats, they gained weight, not surprisingly.  They also had increased acetate levels.  When animals without a gut microbiome were fed the same high fat diet, they did not have increased acetate levels.  This means that the bacteria in the intestine is likely responsible for the increase in acetate.  High levels of acetate increase body weight and triglyceride levels.  (These are regularly checked during your annual checkup with your doctor.)  High acetate levels also signal to the pancreas to make more insulin and to the gastrointestinal system to make more ghrelin, also known as the hunger hormone.  High ghrelin levels increase appetite, and high insulin levels are associated with weight gain.

The good news is that there is a way to intervene!  Scientists altered the microbiome in two ways in animals that had high acetate levels.  The first way was to transplant microbes from healthy animals with normal acetate levels into animals that had high acetate levels from eating high fat food.  The transplant successfully lowered the acetate levels!  The second way to alter the microbiome was to give the animals with high acetate levels a course of antibiotics.  This disrupted the weight gaining signals, and acetate levels returned to normal.  That is not to say that antibiotics are the solution, but it does mean that changing the microbiome or at least the signals it sends through the gut-brain axis is part of the answer.  These findings are a significant step forward, bringing us closer to treating and preventing obesity and metabolic diseases like type 2 diabetes.

If you’re interested in the scientific details, check out the following scholarly article.

Perry RJ, Peng L, Barry NA, Cline GW, Zhang D, Cardone RL, Petersen KF, Kibbey RG, Goodman AL, Shulman GI. Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome. Nature. 2016 Jun 9;534(7606):213-7.

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