Emroy University Did you know that augmented appetite and insulin resistance may be shifted from one mouse to another by means of intestinal bacteria? This discovery seems to reinforce the case that intestinal bacteria may add to human obesity and metabolic disease, as preceding study has apparently demonstrated that intestinal bacterial populations could vary between obese and lean humans. At least this is what a study from Emory University School of Medicine claims.

The first author of the paper, Emory faculty member Matam Vijay-Kumar, PhD, has apparently been investigating a mouse strain with a modified immune system. These mice were said to be engineered to not have a gene, Toll-like receptor 5 (TLR5), which appears to aid cells to feel the existence of bacteria. TLR5 supposedly identifies flagellin, the major constituent of the apparatus that several bacteria utilize to boost themselves.

“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. 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,” commented, Senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine.

The study started with Emory expert Jesse Aitken’s unanticipated inspection that TLR5-deficient mice are roughly 20 percent heavier as opposed to regular mice and encompasses higher triglycerides, cholesterol and blood pressure. They also seemed to have slightly more blood sugar and augmented generation of insulin.

It was seen that apparently TLR5-deficient mice were inclined to have around 10 percent more food as compared to their regular relatives. When their food was limited, they lost weight but still seemed to have reduced reaction to insulin. When fed on a high-fat diet, TLR5-deficient mice apparently put on more weight when pitted against regular mice and, furthermore, contracted full-blown diabetes and fatty liver disease. Supposedly, TLR5-deficient mice seem to display ‘metabolic syndrome,’ a cluster of disorders that in humans augments the threat of suffering from heart disease and diabetes.

Preceding study apparently illustrated that TLR5 seems to play a vital function in controlling bacteria in the intestine. Under specific conditions, several TLR5-deficient mice may contract colitis, an inflammatory bowel disease, while most of the mice apparently suffer from chronic low-level inflammation.

Treating TLR5-deficient mice with powerful antibiotics may decrease their metabolic irregularities. This led Gewirtz’s team to examine the composition of the intestinal bacteria of TLR5-deficient mice, thereby partnering with Ruth Ley at Cornell University. Significantly, Gewirtz and his team discovered that relocating the intestinal bacteria from TLR5-deficient mice to regular mice seemed to shift several of the traits of metabolic syndrome counting augmented appetite, obesity, elevated blood sugar, and insulin resistance.

Gerwirtz remarked, “Even in the absence of colitis, the TLR5-deficient mice seem to have low-level inflammation. We’re not yet sure if this inflammation leads to alterations in intestinal bacteria or vice versa, but this shows that once the microbial community changes, it can transfer metabolic abnormalities to other mice. This suggests that it’s possible to ‘inherit’ metabolic syndrome through the environment, rather than genetically. Do obese children get that way because of bad parenting? Maybe bacteria that increase appetite are playing a part.”

Gewirtz says his team intends to carry out further examinations into variations in the TLR5 gene in humans, and supplementary studies of what’s dissimilar about the bacteria in TLR5-deficient mice and how they could affect appetite and metabolism.

The study was published online in Science magazine.