The world of obesity science is about to be turned on its head. Scientists in Shanghai, China announced in a paper published Dec. 13 that they had isolated a bacterium from a 385-pound man’s intestines, and used it to plump up mice that are specially bred to resist obesity.
They found that the bacteria, a toxin-producing microbe called “enterobacter cloacae,” made up 35 percent of all the microorganisms in the human volunteer’s digestive tract. But a diet formulated specifically to kill off those bacteria succeeded in reducing his levels to below what could be detected in a laboratory.
He lost 113 pounds in 23 weeks.
His high blood pressure disappeared. So did his type-2 diabetes and his fatty liver disease.
The research paper, published online by the International Society for Microbial Ecology’s peer-reviewed “ISME Journal,” is not the first evidence that gut microbes play a significant part in weight gain, but it’s the most convincing to date.
Lead author Zhao Liping, an associate dean of the Shanghai Jiao Tong University’s School of Life Sciences and Biotechnology, made waves when the journal “Science” profiled him in June 2012.
The 200-pound scientist with a 43-inch waist had dropped nearly 45 pounds, he said, with a diet including whole grains and fermented Chinese yams and bitter melons — so-called “prebiotic” foods that can reportedly change the balance of bacteria in the human digestive tract.
A team led by Dr. Jeffrey Gordon, a professor at Washington University in St. Louis, first determined in 2004 that microbes in the intestines could be a major factor in how the body regulates fat storage.
Adult bodies, according to Gordon, contain 10 microbial cells for every human cell. And part of our evolution involved working out a mutually beneficial relationship with all those freeloading bacteria.
Their role, he suggested in that 2004 paper, involved picking up and depositing extra energy from our diets wherever the body needed to store it — usually as fat.
At a press conference Tuesday in Shanghai, according to China Daily, Zhao explained how it works.
“The endotoxin released by the bacterium,” he said, “can activate a gene that helps generate fat. And it also deactivates a gene that consumes fat.”
His team isolated enterobacter microbes from their human subject’s stool samples and mixed them with food given to special “germ free” mice. These blank-slate animals are born in sterile environments where bacteria can’t colonize the digestive system, giving scientists control over what they’re studying.
The bacteria turned the mice into textbook obesity cases, complete with weight gain and signs of diabetes, but only when the animals ate a high-fat diet. Animals on a leaner diet didn’t gain weight — likely because there was no excess energy for the bacteria to convert to fat with its toxins.
Supplemental material distributed to reporters in China included graphs (p. 48) showing a dramatic difference in weight between the bacteria-altered mice and “control” animals given the same diets.
Policy disagreements about the reasons for increasing obesity rates have raged for decades, with public health researchers blaming food producers and restaurant companies for what some call an “obesogenic environment.”
The food industry has blamed a lack of physical activity for the nation’s weight gain, including sedentary behaviors brought on by modern conveniences like automatic dishwashers, television remote controls and public transit systems.
Pharmaceutical companies and those that produce bariatric-surgery equipment, meanwhile, have subsidized public health research examining the depth of the problem and recommending health care and government-entitlement coverage for their branded products.
About 120 million Chinese men, women and children are considered obese, according to the country’s health ministry. In the United States, the latest obesity statistics from the Centers for Disease Control and Prevention suggest that more than 78 million adults are obese, along with about 12.5 million children and adolescents.