The present view of obesity is that it is a combination of sedentary behavior and unwise food choices. Intervention relies on emphasizing activity and altering eating behavior. Recent governmental legislation has been to codify these views. Food and drink choice limitations are now common in public schools. A limit to beverage sizes of fluids thought to promote obesity is now law in New York City and may be initiated by other jurisdictions.
Obesity in our pets is also believed to be a result of the same type of phenomenon; sedentary lifestyle and unwise feeding choices and amounts by owners. There is no question that behavior and diet are important components of obesity. But maybe it isn’t the whole story in this complex problem. Genetic factors or early developmental factors are a major focus of obesity research in humans. Such research is not as common in pets. But a very recent study published in the journal of the International Society for Microbial Ecology is not only fascinating but further emphasizes the complexity of the problem and may impact our approach to the problem in the future.
The Bacteria Study
A common gut bacterium, Enterobacter cloacae, is known to produce a lipopolysaccharide (consists of fat and sugar) toxin that can cause obesity and insulin resistance in mice. In this study the toxin was extracted and purified from enterobacter isolated from the gut of a morbidly obese human subject. The toxin was then administered subcutaneously (under the skin by injection) to a group of germfree mice that were fed a high fat diet.
A second group of germfree mice was also fed a high fat diet and restricted from exercise. The group receiving toxin became obese and insulin resistant while those not receiving toxin did not become obese and develop insulin resistance, despite the diet and lack of exercise. The researchers went one step further and altered the human subject’s diet so that the amount of enterobacter in his gut was reduced from 35% to non-detectable.
In 23 weeks the human subject lost 29% of his body weight and recovered from diabetes and high blood pressure. This is a solitary and very small study, and the findings need to be corroborated by further studies using larger numbers of subjects and different species. And despite the compelling findings, the bacterial toxin is only a factor, not a solitary cause, due to other findings in the study.
Germfree mice in the same study that received the enterobacter toxin but were fed regular mice chow also did not become obese. Also the dietary change for the human subject emphasized whole grains rather than high fat. These findings suggest that the role of bacterial toxin in obesity may be also linked to the amount of fat in the diet.
This study is intriguing in that it further demonstrates the complexity of weight gain and obesity and how much more we need to know to fully understand the problem. Of course, this is true of so many medical and nutritional issues and should remind us that there might be limitations to our simple solutions to solve these problems. It should also remind us to be open to the idea that what may seem true and what appears to be the right decision now may be proven wrong in the future. I love science.
Dr. Ken Tudor
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