By Iris Becene
A recent Johns Hopkins study done on mice suggests the intestinal microbiome is an important factor in the development of obesity and insulin resistance in mammals. Dr. David Hackman from the Johns Hopkins Children’s Center described how past studies suggest that a certain protein, TLR4, may interact with the microbiome to result in metabolic syndrome, which may result in heart attack, stroke, or diabetes. Metabolic syndrome describes an array of conditions including obesity, high blood pressure, and high blood sugar. First, the research team ran an experiment in which half of the mice were genetically modified to lack the TLR4 gene and the other half were the controls. Both groups were fed the same feed for the same period of time. The mice lacking the TLR4 gene developed metabolic syndrome symptoms. Further experiments suggested that deleting the TLR4 gene specifically in intestinal epithelium cells resulted in the greatest effects of metabolic syndrome. Other experiments were completed in which the microbiome of both groups of mice were altered through the ingestion of antibiotics which reduce the amount of bacteria in the intestines. The genetically modified mice that were given antibiotics did not develop metabolic syndrome. Fecal tests showed that bacteria contributing to metabolic syndrome were expressed differently between the genetically modified mice and the control mice. Overall, this study suggests that the interaction of the TLR4 gene and bacterial cells may play a role in metabolic syndrome.
Johns Hopkins Medicine. (2018, February 12). Mouse study adds to evidence linking gut bacteria and obesity. ScienceDaily. Retrieved March 4, 2018 from www.sciencedaily.com/releases/2018/02/180212100618.htm