A high-fat, high-sugar diet alters the composition of bacteria in your intestines, increasing the proportion of the bacteria that make it easier for you gain weight and harder to lose it, according to a November 11, 2009 article in the Los Angeles Times by Thomas H. Maugh II, "High-fat, high-sugar diet alters bacteria in the gut, making it easier to gain weight," regarding research in mice. But does bacteria work the same in humans to make them gain weight and become obese, overriding genetics?
Scientists know obesity runs in families. Now, this study suggests, it may be bacteria alterned by high fat and high sugar diets that can alter the bacteria in your stomach in such as way as to cause rapid weight gain for jsut a small increase in food.
The change in intestinal bacteria can occur in as little as 24 hours, according to November 11, 2009 report in the new journal, Science Translational Medicine. The study is titled, "The Effect of Diet on the Human Gut Microbiome: A Metagenomic Analysis in Humanized Gnotobiotic Mice."
If you're at risk of weight gain, your genetics, physical activity and the environment, are involved along with your diet. According to the LA Times, evidence accumulated by Dr. Jeffrey I. Gordon of Washington University in St. Louis, and other scientiets reveals how intestinal bacteria play a key role. His findings could eventually lead to new ways to induce weight loss or to prevent weight gain in the first place.
Ninety percent of the bacteria in your gut falls into two major divisions, or phyla: the Firmicutes and the Bacteroidetes. Previous research had shown that obese mice had higher levels of Firmicutes, while their lean littermates had more Bacteroidetes.
What the study entailed focused on analyzing the genomes of the bacteria. Researchers found that the firmicutes were more efficient at digesting food that the body can't, such as the complex sugars in grains, fruits and vegetables, breaking them down into simple sugars that can be used by the body.
Animals that have a higher proportion of the more efficient firmicutes in their guts. This type of intestinal bacteria convert a higher proportion of ingested food into calories that can be absorbed by the body, making it easier to gain weight. If you eat just a small increase in absorbed calories for a year, it could lead to a significant amount of weight gain, for example.
What went on in the experiment emphasized transferring bacteria from the guts of obese mice into mice raised in a sterile environment with no bacteria in their guts. These types of mice are called "gnotobiotic mice." Those mice gained more weight than did the mice that were given a similar amount of bacteria from lean mice.
In the experiement, both types of mice at the same diet. Since the experiment had been performed on different types of mice, consumers need to know whether bacteria in the human gut will act the same way.
On November 11, 2009, the research was reported. Scientists concluded that they could transfer bacteria from human intestines into gnotobiotic mice. When the human bacteria went into the intestines of the gnotobiotic mice, the bacteria then were saved as a research tool. Bacteria persists in living. The bacteria colonized the mouse intestines even if the bacteria had been frozen and stored for long periods.
In the experiment, gnotobiotic mice were fed a low-fat, plant-rich diet in the weeks before the bacteria were transplanted and for a month afterward. Analyzing the genomes of the bacteria, the team concluded that the bacterial colony in the mice was virtually identical to that of the human donor.
The important poijnt is the bacteria were transplanted from a lean human donor. What do you think formed?
It was a high proportion of thriving "bacteroidetes" and a low proportion of firmicutes. Then the scientists fed the mice a high sugar, high fat diet. Within 24 hours, the proportions of the two phyla were reversed. With time, the mice also grew fatter than their littermates that did not receive the human bacteria.
Then the bacteria from the fat mice were transplanted into other thin, healthy, gnotobiotic mice. And just as predicted, those mice gained weight on a low-fat diet. Those mice were eating healthy, and they still gained weight. Was it due to the bacteria?
That study suggests the bacterial colonies can be passed from generation to generation, providing an explanation beyond genetics for why obesity runs in families. Was the bacteria contagious? Is that why genetics were bypassed?
The team is now studying bacterial colonies from malnourished children. The outcome of the study is to find out whether the bacterial population can be changed to increase the children's ability to use food.
According to the abstract of the study, "The Effect of Diet on the Human Gut Microbiome: A Metagenomic Analysis in Humanized Gnotobiotic Mice," published in the journal, Science Translational Medicine, "Diet and nutritional status are among the most important modifiable determinants of human health. The nutritional value of food is influenced in part by a person’s gut microbial community (microbiota) and its component genes (microbiome).
"Unraveling the interrelations among diet, the structure and operations of the gut microbiota, and nutrient and energy harvest is confounded by variations in human environmental exposures, microbial ecology, and genotype. To help overcome these problems, we created a well-defined, representative animal model of the human gut ecosystem by transplanting fresh or frozen adult human fecal microbial communities into germ-free C57BL/6J mice.
"Culture-independent metagenomic analysis of the temporal, spatial, and intergenerational patterns of bacterial colonization showed that these humanized mice were stably and heritably colonized and reproduced much of the bacterial diversity of the donor’s microbiota. Switching from a low-fat, plant polysaccharide–rich diet to a high-fat, high-sugar “Western” diet shifted the structure of the microbiota within a single day, changed the representation of metabolic pathways in the microbiome, and altered microbiome gene expression.
"Reciprocal transplants involving various combinations of donor and recipient diets revealed that colonization history influences the initial structure of the microbial community but that these effects can be rapidly altered by diet. Humanized mice fed the Western diet have increased adiposity; this trait is transmissible via microbiota transplantation. Humanized gnotobiotic mice will be useful for conducting proof-of-principle “clinical trials” that test the effects of environmental and genetic factors on the gut microbiota and host physiology."
For further information, see, Science Translational Medince. Another helpful article is "Gut Check: Testing a Role for the Intestinal Microbiome in Human Obesity, J. S. Flier and J. J. Mekalanos, Sci Transl Med 11 November 2009 1:6ps7.
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