The difference between an obese person and a thinner one may not be just diet. Certain microbes that live naturally in our guts may contribute a great deal to whether we become obese and develop obesity-related illnesses such as diabetes. A study published this week demonstrated that a person suffering from obesity was also suffering from extremely elevated levels of a group of gut bacteria called Enterobacter. In fact, Enterobacter comprised 35% of the bacteria in this person's colon.
When Enterobacter die or suffer damage to their cell walls, they release endotoxins, substances that often provoke a strong immune response in other cells. And these immune responses can cause inflammation that tips over into hypertension, diabetes, hyperglycemia, and even colitis.
Once the experimental subject had lost over 50 kg, the amount of Enterobacter in their gut became so small as to be undetectable — and they stopped suffering the effects of hypertension and hyperglycemia. The researchers attribute this transformation to a shift in diet. A high fat diet leads to a population explosion in these bacteria, who release a lot of endotoxins into the body. In their study, the researchers discovered that mice with Enterobacter in their systems rapidly became obese when fed on a high-fat diet; mice with Enterobacter who ate regular chow did not. What this suggests is that Enterobacter could promote obesity in people with a high fat diet, and also might make their obesity far more deadly.
Previously, other research teams have found that high fat diets seem to interact with other gut microbes to cause inflammatory diseases like colitis.
Every human contains millions of microbes throughout our bodies, most of which contribute significantly to keeping us healthy. All those microbes put together are called a microbiome — it's sort of like an ecosystem of microbes. We each have a slightly different microbiome. Scientists have identified several distinct types of human microbiome, and there may be many more. People unlucky enough to have Enterobacter in their microbiomes may be more susceptible to obesity-related diseases, and indeed to obesity itself.
Here is the technical description of what the Enterobacter researchers found, from a paper they published this week in The ISME Journal:
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.
You can read more of the study in The ISME Journal.