Researchers at Joslin Diabetes Centers have identified specific types of gut bacteria that correspond to diabetes, obesity or related metabolic disorders. Previous studies have associated human gut bacteria with various chronic conditions including diabetes and metabolic syndrome.
“Our hope is that if we can identify causal bacteria in these animal models, then we can look in humans for bacteria that serve the same kinds of function,” said Dr. Kahn. “The goal ultimately would be to get a cocktail of purified microbes that is optimized for treatment of humans with obesity or diabetes–kind of a designer probiotic.”
“However, when you change the microbes it has different effects on different mice, depending on the mouse’s genetic background,” Kahn said. “Some animals, and presumably some people, will have much more metabolic syndrome with certain microbes than other animals.”
Three common mouse models had different microbes in their guts. One mouse model was prone to obesity and diabetes, one was prone to obesity but not diabetes, and the third one was resistant to both conditions. A high fat diet changed the microbial population dramatically. The researchers bred new generations of the three different mouse models and tested whether germ-free mice who were given microbes from these three strains of mice were prone to diabetes or obesity like the donors.
Genetic susceptibility to certain bacteria caused chronic health conditions. Diabetes resistant mice gained wight and had higher glucose levels once they were exposed to a transfer of microbes. DNA sequencing identified 3,000 different bacteria in the mouse gut, of which about 300 were fairly abundant. The scientists correlated certain bacterial strains with obesity and high blood glucose levels.
Siegfried Ussar, Nicholas W. Griffin, Olivier Bezy, Shiho Fujisaka, Sara Vienberg, Samir Softic, Luxue Deng, Lynn Bry, Jeffrey I. Gordon, C. Ronald Kahn. Interactions between Gut Microbiota, Host Genetics and Diet Modulate the Predisposition to Obesity and Metabolic Syndrome. Cell Metabolism, 2015; 22 (3): 516 DOI: 10.1016/j.cmet.2015.07.007