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Obesity may influence heart function through sex hormones

Date:
April 28, 2013
Source:
European Society of Endocrinology
Summary:
New research suggests that changes in sex hormones as seen in obesity may have possible effects on the heart. The study suggests effects on heart function in healthy men with artificially raised estrogen levels and artificially lowered testosterone levels to mimic an obese state.

New research suggests that changes in sex hormones as seen in obesity may have possible effects on the heart. The study by researchers from Belgium, presented at the European Congress of Endocrinology in Copenhagen, Denmark, suggests effects on heart function in healthy men with artificially raised estrogen levels and artificially lowered testosterone levels to mimic an obese state.

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Estradiol, an estrogen, is primarily known as a female hormone but it also circulates at very low levels in men. Testosterone is converted to estradiol by the enzyme aromatase, the activity of which might be increased in obesity leading to raised estradiol and reduced testosterone.

To determine whether obesity might alter heart function via changes in sex hormones, Drs Maarten De Smet and colleagues at Ghent University in Belgium recruited 20 healthy men aged 20-40 and used an aromatase inhibitor and an estrogen patch to artificially alter the hormone levels to mimic sex hormone concentrations in obesity (high estradiol and low testosterone) vs contrast by an aromatase inhibitor (low estradiol, high testosterone). Prof Dr T De Backer, Cardiologist, assessed the heart function before and seven days after the intervention using ultrasonographic imaging with strain analysis, which measures the deformation of the heart between the resting and contracted states.

The men with obesity-related changes in sex hormones exhibited altered heart function. At baseline the global circumferential strain was -17.1% +/-3.9, which decreased significantly to -14% +/-2.5 (p=0.01). The contrasting group did not show any difference.

By artificially altering sex hormones in a small number of healthy men, Drs De Smet and colleagues have shown that an altered sex hormone profile as seen in obesity might be relevant for heart function. Adequately powered clinical trials with sufficient duration may establish the role of sex hormones in the heart function of obese men.

Maarten De Smet, Masters student in Medicine at Ghent University, Belgium, and first author said:

"Obesity is a major contributor to heart disease. By giving an aromatase inhibitor and estrogen to healthy men we mimicked the effect of sex hormones in obesity alone, in isolation from the rest of the obese metabolic state.

"In order to pump blood around the body the heart must fill with blood and then contract, pushing the blood out. We found that after increasing the estrogen levels and decreasing the testosterone levels in men for one week the deformation of the left heart chamber was significantly altered.

"Because the contributing factors to obesity, as well as the underlying biology, are so complicated it's a real challenge to tease apart one single aspect, so we think this study is of particular interest. As these results are from a small number of healthy men over one week, we hope to investigate sex hormone changes and the heart in the obese in the long term."


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The above story is based on materials provided by European Society of Endocrinology. Note: Materials may be edited for content and length.


Cite This Page:

European Society of Endocrinology. "Obesity may influence heart function through sex hormones." ScienceDaily. ScienceDaily, 28 April 2013. <www.sciencedaily.com/releases/2013/04/130428144857.htm>.
European Society of Endocrinology. (2013, April 28). Obesity may influence heart function through sex hormones. ScienceDaily. Retrieved April 1, 2015 from www.sciencedaily.com/releases/2013/04/130428144857.htm
European Society of Endocrinology. "Obesity may influence heart function through sex hormones." ScienceDaily. www.sciencedaily.com/releases/2013/04/130428144857.htm (accessed April 1, 2015).

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