Enterobacter and Obesity

ISME Journal Dec 13, 2012 has an article by Chinese researchers reporting evidence that a diet which makes the pH of the gut more acidic changes the bacterial composition of the gut, decreasing the population of enterobacter to non-detectable levels. Decreasing the number of bacteria also reduces the toxin produced by the bacteria. The toxin causes insulin resistance and weight gain.

An obese subject who was put on a diet of whole grains, traditional Chinese medicinal foods, and probiotics for 23 weeks lost 51 kg, which is a bit more than the amount of weight lost after weight-loss surgery. The subject did not change the amount of exercise he did.

The Chinese researchers took bacteria from the obese man before the diet and fed them to rats, after which the rats began to gain weight.



Abstract:

Lipopolysaccharide endotoxin is the only known bacterial product which, when subcutaneously infused into mice in its purified form, can induce obesity and insulin resistance via an inflammation-mediated pathway. Here we show that one endotoxin-producing bacterium isolated from a morbidly obese human’s gut induced obesity and insulin resistance in germfree mice. The endotoxin-producing Enterobacter decreased in relative abundance from 35% of the volunteer’s gut bacteria to non-detectable, during which time the volunteer lost 51.4 kg of 174.8 kg initial weight and recovered from hyperglycemia and hypertension after 23 weeks on a diet of whole grains, traditional Chinese medicinal foods and prebiotics. A decreased abundance of endotoxin biosynthetic genes in the gut of the volunteer was correlated with a decreased circulating endotoxin load and alleviated inflammation. Mono-association of germfree C57BL/6J mice with strain Enterobacter cloacae B29 isolated from the volunteer’s gut induced fully developed obesity and insulin resistance on a high-fat diet but not on normal chow diet, whereas the germfree control mice on a high-fat diet did not exhibit the same disease phenotypes. The Enterobacter-induced obese mice showed increased serum endotoxin load and aggravated inflammatory conditions. The obesity-inducing capacity of this human-derived endotoxin producer in gnotobiotic mice suggests that it may causatively contribute to the development of obesity in its human host.