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Estrogen A Possible Factor In Obesity – For Both Sexes, Researchers Say

Date:
November 7, 2000
Source:
University Of Illinois At Urbana-Champaign
Summary:
Estrogen – even in men – may weigh in as a component in the regulation of obesity, along with other well-known risk factors such as food indulgence and lack of exercise, according to researchers at two universities.

CHAMPAIGN, Ill. — Estrogen – even in men – may weigh in as a component in the regulation of obesity, along with other well-known risk factors such as food indulgence and lack of exercise, according to researchers at two universities.

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In the Nov. 7 issue of the Proceedings of the National Academy of Sciences, the scientists report that male mice genetically altered to lack one type of estrogen receptor became obese, expended less energy and built up larger stores of fat, even though they were fed the same as normal mice.

“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 University of Illinois College of Veterinary Medicine. “Our findings suggest that estrogen may be important for regulating fat in men as well as women.”

According to the World Health Organization, more than 60 percent of the adult population of the United States is overweight and a growing number of adults are obese. The problem is mirrored in other developed nations. Also rising are rates of Type 2 diabetes, which is closely linked to obesity; the health organization projects the number of sufferers will double by 2010.

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.” The researchers also theorize that estrogen signaling may be important for the normal development and function of white adipose tissue in males.

Co-authors of the PNAS paper were Heine, departmental colleague Paul S. Cooke, Gary A. Iwamoto, a UI professor of kinesiology, and J.A. Taylor and D.B. Lubahn, both of the University of Missouri in Columbia. Their 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.


Story Source:

The above story is based on materials provided by University Of Illinois At Urbana-Champaign. Note: Materials may be edited for content and length.


Cite This Page:

University Of Illinois At Urbana-Champaign. "Estrogen A Possible Factor In Obesity – For Both Sexes, Researchers Say." ScienceDaily. ScienceDaily, 7 November 2000. <www.sciencedaily.com/releases/2000/11/001107065552.htm>.
University Of Illinois At Urbana-Champaign. (2000, November 7). Estrogen A Possible Factor In Obesity – For Both Sexes, Researchers Say. ScienceDaily. Retrieved January 27, 2015 from www.sciencedaily.com/releases/2000/11/001107065552.htm
University Of Illinois At Urbana-Champaign. "Estrogen A Possible Factor In Obesity – For Both Sexes, Researchers Say." ScienceDaily. www.sciencedaily.com/releases/2000/11/001107065552.htm (accessed January 27, 2015).

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