Gut Bugs may explain obesity-cancer link

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Gut Bugs may explain obesity-cancer link -

risk. changes in the gut flora may help explain why obese mice are more likely to develop liver tumors ( insert ).

Eiji Hara Foundation / Japanese for Cancer Research

Why obesity increases the risk of developing cancer? A new study suggests that the wrong mix of intestinal bacteria may be to blame. The researchers report that the obese mice carry the modified insect intestinal communities, which produce acid damaging DNA which leave mice more susceptible to liver cancer. The results suggest that bacteria help the development of the drive cancer and may eventually help scientists better predict and prevent disease.

Obesity increases the chances of becoming a victim of some types of cancer, including colorectal and liver tumors, but scientists have not been able to identify the mechanism behind this link. They suspected that our gut microbiota, the complex community of trillions of microbes living in our intestines, play a role. After all, the markers of the intestine have been linked to other diseases, including inflammatory bowel disease, allergies, and even heart disease, and are known to vary between thin and obese individuals.

Eiji Hara molecular biologist from the Institute of Cancer at the Japanese Foundation for Cancer Research in Tokyo and colleagues set out to connect the dots between cancer and intestinal microbes by studying the development of cancer in obese and lean mice. They started with two groups of mice: Lean mice that grew up on a normal diet and mice that ate a diet heavy in fat until they were obese. To encourage rodents to develop cancer- "Mice do not smoke or drink alcohol, so they are quite without cancer," Hara said they exposed the animals to a chemical carcinogen shortly after birth.

The mice showed the same link to obesity cancer observed in humans and other animals. Only 5% of lean mice exposed to the carcinogen developed cancer later in life, while all obese mice did. When the researchers repeated the experiment using high mouse to be obese even on a normal diet, they also saw an increased incidence of cancer, suggesting that obesity itself, and not "the animal diet increased their risk of cancer.

obese mice were prone to liver cancer, their tumors showed high concentrations of molecules called pro-inflammatory cytokines which trigger inflammation. the obese mice also had higher levels of deoxycholic acid (DCA), a by-product remaining after certain intestinal microbes break bile acids produced by the liver. DCA damages DNA and has been associated with certain cancers in humans.

to trace the origins of these two signs, the presence of inflammatory cytokines and promoting higher levels of DCA-the researchers scrutinized the entrails of animals. They found that obese mice received a different mix of bacteria. So-called gram-positive bacterial strains, in particular, seemed to thrive in luscious mouse. When Hara and colleagues treated mice with vancomycin, an antibiotic that targets Gram-positive bacteria, the animals showed a reduction in cancer incidence and levels of DCA. Furthermore, by directly reducing the DCA levels of animals (more stimulating the secretion of bile acid or slow distribution of bile acids) also reduces the risk of cancer, and giving them extra DCA increased their risk, reports online today in team Nature .

Together, the results suggest that obesity causes a domino effect causing cancer in which DCA is key, says Hara. Changes gut microbiota, stimulating populations of gut microbes that produce more than DCA. Then, the excess of DCA causes DNA damage and inflammation in the liver, which in turn leads to liver cancer.

"I am very surprised by the process," said Hara. "We did not expect that changes in the gut microbiota could cause increased risk of cancer."

"I think this study is very exciting, "said Peter Turnbaugh, a Harvard University microbiologist who was not involved in the work. "It was a mystery for a while why obesity leads to a higher risk of cancer. They convincingly that the microbial community is involved. "

Turnbaugh notes that more research is needed to show that a similar mechanism is at work in humans. But if it is, the results could pave the way for better methods of prediction and prevention of cancer. Changes DCA levels, for example, could allow doctors to assess the risk of cancer and to take measures for prevention, he said.

"If it is true that the production of this acid leads to cancer, there may be ways to inhibit production by manipulating microbial communities of diet or fine tuning people," says Turnbaugh. "But there is certainly much more to learn first."

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