Pathologist Andrew Gewirtz and his colleagues have been getting some well–deserved attention for their research on intestinal bacteria and obesity.
Briefly, they found that increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria. The results were published online by Science magazine.
Previous research indicated intestinal bacteria could modify absorption of calories, but Gewirtz and his colleagues showed that they influence appetite and metabolism (in mice)
“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,” Gewirtz says. “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.”
A related report in Nature illustrates how “next generation” gene sequencing is driving large advances in our understanding of all the things the bacteria in our intestines do to us.
Gewirtz’s laboratory’s discovery grew out of their study of mice with an altered immune system. The mice were engineered to lack a gene, Toll-like receptor 5 (TLR5), which helps cells sense the presence of bacteria.
TLR5-deficient mice are about 20 percent heavier than regular mice and have elevated triglycerides, cholesterol and blood pressure. They tend to consume about 10 percent more food than their regular relatives, and have elevated blood sugar and increased production of insulin. In short, TLR5-deficient mice have “metabolic syndrome,†a cluster of disorders that in humans can lead to heart disease and diabetes.
In collaboration with Ruth Ley at Cornell University (a leader in the genetic study of bacteria in people), Gewirtz’s team found that TLR5-deficient mice had an altered set of the bacterial species in their intestines. Ley’s research has previously shown that intestinal bacterial populations differ between obese and lean humans.
Under certain conditions, many TLR5-deficient mice develop inflammatory bowel disease, while the majority of the mice have chronic low-level inflammation, which may dampen their bodies’ response to insulin.
Treating TLR5-deficient mice with strong antibiotics, enough to kill most of the bacteria in the intestine, reduces their metabolic abnormalities.
As a final proof of the power of intestinal bacteria, transferring bugs from TLR5-deficient mice to regular mice, after they were first treated with antibiotics, could confer many of the characteristics of metabolic syndrome including increased appetite, obesity, elevated blood sugar, and insulin resistance.
Gewirtz’s team plans additional research on humans’ intestinal bacterial populations, which are thought to be relatively stable after acquisition at birth from family members.
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