Study: Intestinal Bacteria May Be Causing Obesity

Recently released results of Scientific research suggests that bacteria in your intestines may be playing an important role in how the body stores foods you eat and how it affects your weight

Recently released results of Scientific research led by Andrew Gewirtz at Emory University reportedly reveals that bacteria in your intestines -- so-called gut microbiota -- may play an important role in how your body stores the foods you eat and how it affects your weight. Gewirtz's team and researchers at Emory, Cornell University and the University of Colorado at Boulder became interested in the relationship between intestinal bugs and weight when they noticed lab mice lacking a certain protein had more bugs than other animals and were almost 15% heavier. Mice that were lacking a certain protein had a higher level of inflammation that researchers say may account for the extra weight. Metabolic syndrome can be promoted by inflammatory signaling, causing weight gain, high blood pressure and high cholesterol levels, and a higher risk of developing diabetes and heart disease. The heavier mice in Gewirtz's study were bred to lack a protein known as toll-like receptor 5 (TLR5), which is sprouted on the surface of most intestinal cells. TLR5's job is recognizing and binding to the whip-like flagella that bacteria use to move around, in essence acting as a traffic cop for controlling masses of pathogens that live in the intestine; without it, normally harmless gut bacteria tend to over flourish and expand in number. Symptoms of Metabolic Syndrome Present in TLR5-Deficient Mice The study found that when that happens, it triggers an inflammatory state as the body tries to respond to the increasing population of bugs, while at the same time it makes cells less sensitive to insulin, which in a way, competes with inflammatory factors for the attention of the same intestinal cells; if the cells are responding to inflammatory factors, they are less likely to take up glucose and effectively process it. A desensitization to insulin and glucose then leads to the symptoms of metabolic syndrome, such as weight gain, high triglyceride levels and cholesterol, and elevated blood pressure -- all of which were present in the TLR5-deficient mice. Gewirtz doesn't think the bacteria directly makes the mice eat more, but the bacteria are causing low-grade inflammation, causing insulin resistance that then make the mice eat more. Researchers conducted a series of experiments to test that theory, the most illuminating of which revealed that when TLR5-deficient mice were given unrestricted diets, they consumed 10% more than normal mice. Even when their food was limited, the mice were still less sensitive to insulin than their normal counterparts. People May Be Eating More Due to Changes in Their Intestinal Bacteria When the team transferred the bacterial gut population from TLR5-deficient mice into animals that were specifically bred to have no immune system -- making them incapable of rejecting foreign cells and bacteria -- the finding was confirmed. When those animals received the teeming bacteria from the TLR5-deficient mice, they also began eating more and developed the same metabolic-syndrome symptoms their donors had. In essence, the obesity profile of the heavier mice was transferred to the normal mice. The results suggest that one reason people might be eating more is because of changes in their intestinal bacteria according to Gewirtz. What causes changes in gut microbiota? Gewirtz says that many things, including the use of antibiotics, cleaner water and improved sanitation and hygiene in general, which influences the type and amount of microbes residing in the intestines. The study found that in TLR5-deficient animals, the total percentage of 150 species of bacteria in the gut was three to four times higher than those those in normal mice while 125 other types of bacteria were less common. Findings Limited to Mice, but May Be Applicable to Humans It's not yet known which is more important -- that some of those species are missing or that some are in greater abundance -- but the net effect is that in the absence of TLR5, the microbe community changes, and when the intestinal bacteria changes, the host response changes too, which may predispose you to a variety of diseases of which obesity and metabolic syndrome are perhaps the most mild according to Gewirtz. The next step for scientists wanting to understand the precise link between intestinal microbiota and obesity is studying those changes. According to the report, an important part of that investigation involves having an accurate map of the genetic makeup of those gut bugs. A separate, recently published paper by an international group of scientists generated the most comprehensive map to date of human gut microbes, using 124 human fecal samples, which gives scientists the critical window they need to figure out which species of bugs tend to reside in our intestines and which may contribute to weight gain. Gewirtz's findings are limited to mice, but experts believe they may be just as applicable to humans because previous studies on gut microbiota found that obese people tended to have a makeup of intestinal pathogens that were different from those of people of normal weight. Gewirtz says the results suggest that the tendency to eat more may not only be driven by the fact that food is cheaper and more available. It may be due to a change in the bacteria in the intestines. A low-grade inflammation some people have which could be due to changes in their gut bacteria may be making people eat too much. If it's true, as noted by the report, then studies like this one could open new doors into understanding the myriad ways that pathogens like bacteria can cause disease, including methods that have nothing to do with infection.