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AN OBESITY VIRUS?
By Sean Henahan, Access Excellence NEW ORLEANS (4/07/97) Is obesity caused by a virus? New virological and biochemical findings could lead to new treatment approaches for obesity, according to reports at the annual meeting of the Federation of American Societies for Experimental Biology. University of Wisconsin researchers report that as many as 15% of obese people carry antibodies to a form of adenovirus (Ad-36) that has been implicated in obesity in other animals. The researchers tested 154 obese and 45 lean human volunteers for the presence of antibodies to Ad-36. He found about 15 percent of the obese volunteers had antibodies to Ad-36 while the lean volunteers showed none. The antibody-positive obese people had significantly lower cholesterol and triglycerides levels than the antibody-negative obese people, a pattern similar to that seen in animals infected with Ad-36. But the two groups did not differ on any of 29 other measures the researchers compared, including age or family history of obesity. In male patients in particular, the presence of antibodies was associated with a significantly better response to treatment with obesity drugs Between 80 and 90 million Americans are obese, defined as having a body-mass index of 27 or above. Body mass index is calculated by dividing a person's weight in kilograms by the square of height in meters. A viral connection to obesity in humans has never been seriously considered before, the researchers noted. "There has been an alarming worldwide increase in the prevalence of obesity in the past 30 years," said Richard Atkinson, Professor of Medicine and Nutritional Science at the University of Wisconsin, noting that its prevalence in the United States rose 30 percent between 1980 and 1990, affecting more than 33 percent of the population. "This increase is the type of pattern that might occur with a new infectious disease, as has been seen with the AIDS virus. A great deal of further research is necessary to determine if the global epidemic of obesity may be due in part to infection with Ad-36," he said. The studies began after Dr. Nikhil Dhurandhar found that one type of adenovirus that infects birds and is found only in his native India could induce obesity when it was injected into chickens.Dhurandhar and Atkinson next injected laboratory animals with a form of adenovirus known to affect humans, Ad-36, which resulted in obesity. Human adenoviruses form a large family of some 50 viruses. Transmitted through the air, they can cause upper respiratory infections, cold symptoms, gastrointestinal problems and eye inflammation in humans. "A paradoxical characteristic of the virus is that in animals it appears to produce low levels of cholesterol and triglycerides along with the obesity," said Dhurandhar, noting that obesity is usually accompanied by elevated levels of these substances. In a related presentation, researchers from the University of Buffalo proposed a novel biochemical explanation for obesity that could also aid development of treatments for the condition. The researchers detailed research with rat pups that has shown that different tissues exhibit specific responses to hyperinsulinemia, the overproduction of insulin that occurs in obesity. Unlike previous animal models in which both conditions occur simultaneously, the UB model is the first to demonstrate that chronic hyperinsulinemia precedes obesity. Working with rat pups born to mothers who were hyperinsulinemic and obese, the researchers measured the effect of chronic hyperinsulinemia on key enzymes in the insulin-signaling pathway. "Our results show that in the presence of an overproduction of insulin, obesity develops because while the functional activity of the insulin-signal transduction pathway is decreased in liver and muscle tissue, its activity is increased in fatty tissue," said Mulchand S. Patel, Ph.D., professor and chair of the UB Department of Biochemistry "This information provides a biochemical basis for the development of obesity and may make it possible one day to develop specific interventions for obesity." The findings suggests the rat pups have an early metabolic setpoint, which programs them to overproduce insulin early in life and become obese later on. Normally, insulin is produced by the pancreas in varying levels, depending on the amount of glucose in the blood. But while in utero, the pancreatic cells of these offspring somehow are targeted to overproduce insulin by hormonal or environmental influences from the mothers, who are hyperinsulinemic and obese, said Patel. "The pancreatic cells in the pups respond to the hyperinsulinemia in the mothers early on, and later in adult life, the body responds to the offspring's hyperinsulinemia. It's a big mystery as to how this happens because these second-generation animals experience no dietary modification," Patel said. He noted that the rat pups' only risk factor is that they were born to hyperinsulinemic mothers. "In our study, second generation rats express hyperinsulinemia early in the post-weaning period, as their mothers did," stated Patel. "In spite of the fact that they were not eating a high-carbohydrate diet, the pups' metabolic setpoint may have a similar pattern to the mothers'." The researchers now are trying to pinpoint exactly how early in their lives the rats begin to exhibit hyperinsulinemia and whether or not they are born with it. Both studies were presented their findings at the Experimental Biology annual meeting, April 7, 1997. Related information on the Internet
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