RESEARCH General Health

BIOLOGY
Estrogen a possible factor in obesity -- for both sexes, researchers say

Jim Barlow, Life Sciences Editor
(217) 333-5802; b-james3@uiuc.edu

12/1/2000

CHAMPAIGN, Ill. -- Estrogen -- even in men -- may join food indulgence and lack of exercise as factors affecting obesity, researchers on two continents say.

That conclusion is drawn from two companion papers published in the Nov. 7 issue of the Proceedings of the National Academy of Sciences. In the studies, male mice that had been genetically altered to lack either one type of estrogen receptor or the ability to produce estrogen became obese when fed the same amounts as normal mice, expended less energy and built up larger stores of fat.

Scientists from the University of Illinois and University of Missouri did one study; researchers at Prince Henry's Institute in Australia did the other.

"Male mice without the receptor for the classical form of estrogen, which has always been considered a female hormone, got fatter than wild-type mice," said Patricia A. Heine, a professor in the department of biosciences in the UI College of Veterinary Medicine. "Our findings suggest that estrogen may be important for regulating fat in men as well as women," said Paul S. Cooke, a departmental colleague and co-lead investigator.

Australian researchers, led by Margaret Jones and Evan Simpson, reached similar conclusions after observing that male mice genetically engineered to lack estrogen also became obese.

The World Health Organization estimates that more than 60 percent of the adult population of the United States is overweight and a growing number of adults are obese -- a problem that is mirrored in other developed nations. Also rising are rates of Type 2 diabetes, which is closely linked to obesity.

Using the genetically altered mice and normal wild-type mice, researchers studied the effects of estrogen on various tissues in both males and females. In the altered mice, they saw a rise of up to 170 percent in the amount of fat, becoming apparent first at 30 days of age and increasing through one year of age. In addition, the estrogen-deficient mice had an 11 percent decrease in energy expenditure.

"The increase in fat," Heine said, "was due to both an increase in the size of the individual cells making up the fat, as well as the number of cells present." The lack of estrogen led to an increase in white adipose tissue, as well as insulin resistance and glucose intolerance. Such a relationship was known to occur in female mice and post-menopausal women, but it had not been shown in males.

"In light of the metabolic results of our study, it appears that estrogen enhances one's ability to burn excess fat in both males and females," Heine said. "We don't know yet if the lack of estrogen is merely decreasing the basal metabolic rate, or if it is also decreasing the activity level of mice."

Co-authors with Heine and Cooke were Gary A. Iwamoto, a UI professor of kinesiology, and J.A. Taylor and D.B. Lubahn of the University of Missouri in Columbia. The work was supported by grants from the National Institutes of Health and the Animal Health and Disease Research Funds of the UI Agricultural Experiment Station.