One factor thought to contribute to this rise is obesity of the mother during pregnancy. However, a team of researchers, at Oregon Health and Science University, Beaverton, and the University of Colorado School of Medicine, Aurora, have found the offspring of both lean and obese nonhuman primate mothers chronically consuming a high-fat diet exhibited an increased risk of developing NAFLD. Importantly, if mothers fed a high-fat diet were reverted to a low-fat diet during a subsequent pregnancy, this second offspring exhibited fewer signs of NAFLD. The team, led by Kevin Grove and Jacob Friedman, therefore suggests that a developing fetus is highly susceptible to maternal consumption of excess fat, whether or not the mother is obese, and that a healthy maternal diet is most important for the obesity-related health of a developing fetus.

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The team's study is the first molecular survey of gut microbial diversity following surgical weight loss, and has helped solidify the link between methane producing microbes and obesity. Specifically, the microbial populations extracted from obese individuals were high in a particular microbial subgroup, hydrogen-producing bacteria known as prevotellaceae. Further, such hydrogen producers appear to coexist with hydrogen-consuming methanogens, found in abundance in obese patients, but absent in both normal weight and gastric bypass samples. Unlike the hydrogen producers, however, these methane-liberating hydrogen consumers are not bacteria. They belong instead to the third great microbial domain ”the Archaea, (with Eukarya and Bacteria making up the other two).

Energy managers

During the course of digestion, calories are extracted from food and stored in fat tissue for later use ”a process delicately regulated by the multitude of microbial custodians. The intermediary products of the digestive process include hydrogen, carbon dioxide and several short chain fatty acids (SCFAs).

Results suggest a cooperative co-existence in obese individuals between hydrogen-producers and hydrogen consuming methanogens. Rittmann explains how this mutually reinforcing relationship, known as syntrophy, may contribute to obesity:

"Organisms producing hydrogen and acetate create a situation like cars flooding onto the highway. The methanogens, which remove the hydrogen, are like the offramps, allowing the hydrogen cars to get off. That allows more acetate cars to get on, because some hydrogen cars are coming off the highway."

The methanogen offramps, by removing hydrogen, accelerate the efficient fermentation of otherwise indigestible plant polysaccharides and carbohydrates. The effect is to boost production of SCFAs, particularly acetate, which will be taken up by the intestinal epithelium and converted to fat. The result over time may be increasing weight, eventually leading to obesity.

While weight regulation involves a complex interplay of genetic predisposition, exercise, eating habits, and other factors, manipulation of the gut's microflora, particularly the methanogenic Archaea, may provide additional avenues for the treatment of morbid obesity.

The researchers stress that the study is preliminary, but were encouraged by the findings from their small sample. Future investigation is needed to establish the differences in composition of gut microbiota across different age groups and under varying weight-loss regimens involving diet and exercise. Nevertheless, the study's findings point to new avenues for modifying the body's energy harvesting efficiency ”perhaps by manipulation of the Bacteria-Archaea nexus.

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