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Intestinal Bacteria


Elite121

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http://www.sciencedaily.com/releases/20 ... 142232.htm

Found this to be a fascinating read today:

The finding strengthens the case that intestinal bacteria can contribute to human obesity and metabolic disease, since previous research has shown that intestinal bacterial populations differ between obese and lean humans.

"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost high-calorie foods," says senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine. "However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism."The first author of the paper is Emory faculty member Matam Vijay-Kumar, PhD, who has been studying a mouse strain with an altered immune system. These mice were engineered to lack a gene, Toll-like receptor 5 (TLR5), which helps cells sense the presence of bacteria. TLR5 recognizes flagellin, the main component of the apparatus (flagella) that many bacteria use to propel themselves.

The study began with Emory researcher Jesse Aitken's unexpected observation that TLR5-deficient mice are about 20 percent heavier than regular mice and have elevated triglycerides, cholesterol and blood pressure. They also have mildly elevated blood sugar and increased production of insulin, Vijay-Kumar and Gewirtz found. TLR5-deficient mice tended to consume about 10 percent more food than their regular relatives. When their food was restricted they lost weight but still had a decreased response to insulin (i.e. insulin resistance). When fed a high-fat diet, TLR5-deficient mice gained more weight than regular mice and, moreover, developed full-blown diabetes and fatty liver disease. In short, TLR5-deficient mice exhibit "metabolic syndrome," a cluster of disorders that in humans increases the risk of developing heart disease and diabetes.Previous research has shown that TLR5 plays a prominent role in controlling bacteria in the intestine. Under certain conditions, many TLR5-deficient mice develop colitis, an inflammatory bowel disease, while the majority of the mice have chronic low-level inflammation.

"The intestine is like a complex community, with good and bad actors," Gewirtz says. "We can think of TLR5 as being like a neighborhood police officer who can distinguish law-abiding residents from potential trouble makers. Take away TLR5, and the safety of the community deteriorates."

Treating TLR5-deficient mice with strong antibiotics, enough to kill most of the bacteria in the intestine, reduces their metabolic abnormalities. This led Gewirtz's team to analyze the composition of the intestinal bacteria of TLR5-deficient mice, collaborating with Ruth Ley at Cornell University.

Ley's earlier research on mice and humans shows that obesity results in more bacteria of the Firmicutes family and less of the Bacteroidetes, which increases the intestine's ability to harvest calories from food. In contrast, TLR5-deficient mice had normal proportions of Firmicutes and Bacteroidetes but differed in the bacterial species that comprised these families.

Importantly, Gewirtz and his team found that transfer of the intestinal bacteria from TLR5-deficient mice to regular mice transferred many of the characteristics of metabolic syndrome including increased appetite, obesity, elevated blood sugar, and insulin resistance.Humans' intestinal bacterial populations are thought to be acquired at birth from family members and are relatively stable, but they can be influenced by diet and antibiotics.

"Previous research has suggested that bacteria can influence how well energy is absorbed from food, but these findings demonstrate that intestinal bacteria can actually influence appetite," Gewirtz says.Noting that insulin is known to dampen appetite, he adds: "Even in the absence of colitis, the TLR5-deficient mice seem to have low-level inflammation. We're not yet sure if this inflammation leads to alterations in intestinal bacteria or vice versa, but this shows that once the microbial community changes, it can transfer metabolic abnormalities to other mice. This suggests that it's possible to 'inherit' metabolic syndrome through the environment, rather than genetically. Do obese children get that way because of bad parenting? Maybe bacteria that increase appetite are playing a part."

Gewirtz says his team plans future investigations into variations in the TLR5 gene in humans, and additional studies of what's different about the bacteria in TLR5-deficient mice and how they might influence appetite and metabolism.The research was supported by the National Institutes of Health and the Crohn's and Colitis Foundation of America.

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So the bacteria are causing people to gain weight? Interesting. Thanks for posting, Elite.

By the looks of things it may very well be possibility, I'm sure in time we will learn more, I'm not intelligent enough to break that info down...but there is so much more about our human bodies that we just don"t know.

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My first thought was that it wasn't what I'd have expected. I'd have thought bacteria aid digestion, so we process food more efficiently. But then I realised that processing food more efficiently probably means more nutrients to store - hence fat gain. So yeah, it does make sense.

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My first thought was that it wasn't what I'd have expected. I'd have thought bacteria aid digestion, so we process food more efficiently. But then I realised that processing food more efficiently probably means more nutrients to store - hence fat gain. So yeah, it does make sense.

Just finished reading "Why Stomach Acid is Good For You..if anyone is interested in how the digestive system works, and just how mislead we have become, I highly recommend this book, one thing that is becoming apparent to me is that digestion is an often overlooked factor in peoples health...as the old saying goes "Death Begins In The Colon"

The other bacteria I have reading about is Helicobacter pylori, and its affects on weight-gain as well as its other effects on the body. One thing for sure is that by eating C.R.A.P ((Caffiene, Refinded/Processed foods, Alcohol/Aspartame, and Pasteurized milk), according to what I've read all have a part to play in increasing unfriendly gut bacteria...then there is also the issue whereas the bacteria feeds off of the C.R.A.P foods and excrete toxins that compromise"s ones immunity severely...

Sorry know its a little off topic what Ive posted here.

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I can't understand why scientists are delving in to complex issues to explain such a simple concept

"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost high-calorie foods," says senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine. "However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism."

Does this mean people are forced to eat shit, live a sedentary lifestyle and do nothing to help themselves? and blame a "metabolic disease" for being fat? :doh:

People are fat because they choose to be fat end of story

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Funny video....and also agree people need to take more responsibility for their health & wellbeing, I merely pointed this article out as a topic of interest..lets say that if someone is dieting & exercising, and still not losing weight there might be an underlying cause not addressed such as an intestinal bacteria infection.

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I agree mate, it just really rials me up when something can be potentially interpreted by fat lazy people as justification for being... well fat and lazy :lol:

Nicely said there... yeah it is frustrating....some people are just not prepared to make the effort to change.....as the saying goes "More Of The Same Equals More Of The Same"

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I agree mate, it just really rials me up when something can be potentially interpreted by fat lazy people as justification for being... well fat and lazy :lol:

Nicely said there... yeah it is frustrating....some people are just not prepared to make the effort to change.....as the saying goes "More Of The Same Equals More Of The Same"

My favorite is "The definition of stupidity is doing the same thing over and over again and expecting different results"

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