Are belly bacteria making us overeat?

- Monday, March 29, 2010

Recent research suggesting that intestinal bacteria may actually change the host person’s appetite and insulin resistance.

I’m curious what effect fasting and/or cleanse diets have on these bacteria colonies, and if foods like yogurt and other ‘good bacteria’ foods can have significant positive effect.

Intestinal bacteria also may play a role in human obesity and metabolic disease.

A new study shows that increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria.

Previous research has shown that intestinal bacterial populations differ between obese and lean humans.

“It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost, high-calorie foods,” says senior author Andrew Gewirtz, associate professor of pathology and laboratory medicine at Emory University School of Medicine.

“However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism.”

The study is published online in _Science _magazine.

Emory faculty member Matam Vijay Kumar has been studying mice with an altered immune system that were engineered to lack Toll-like receptor 5 (TLR5), a gene that helps cells sense the presence of bacteria.

TLR5 recognizes flagellin, the main component of the apparatus (flagella) that many bacteria use to propel themselves.

The TLR5-deficient mice were about 20 percent heavier than regular mice and had elevated triglycerides, cholesterol, and blood pressure, and mildly elevated blood sugar and increased production of insulin.

TLR5-deficient mice consumed about 10 percent more food than their regular relatives. When their food was restricted they lost weight but still had a decreased response to insulin (i.e. insulin resistance).

When fed a high-fat diet, TLR5-deficient mice gained more weight than regular mice and, moreover, developed full-blown diabetes and fatty liver disease.

In short, TLR5-deficient mice exhibit “metabolic syndrome,” a cluster of disorders that in humans increases the risk of developing heart disease and diabetes.