Abstract
Menopause-related hormonal changes are associated with an increased prevalence of various cardiometabolic risk factors, components of the metabolic syndrome, and an excess risk of all-cause and cardiovascular mortality. Estrogen withdrawal and the subsequent androgenicity interact in a synergistic manner to predispose post menopausal women to an increase in total body weight but also to a pronounced change of body composition. Central fat accumulation and ectopic fat storage constitute potent determinants of the increased cardiometabolic risk in post menopausal women. In contrast, peripheral subcutaneous fat has an independent cardioprotective and anti-atherogenic impact. Data are less conclusive regarding the contribution of lean body mass to metabolic syndrome and cardiometabolic health in post menopausal women.
Highlights
Menopause constitutes a transitional period from reproductive to non-reproductive life, which is mainly characterized by a major reduction in estrogens production and androgenicity [1]
Total body fat mass as well as its regional distribution, consisting of central fat accumulation, decreased peripheral fat mass and ectopic fat storage, constitute potent determinants of the increased prevalence of metabolic syndrome (MS) in Post menopausal women (PMP) women [46], whereas data are less conclusive regarding the contribution of lean body mass [7]
In addition to an evident increase in total fat mass, a remarkable change in body composition is observed in menopause, which is mainly characterized by a marked increase in subcutaneous and visceral abdominal fat and a concomitant reduction in lean body mass (LBM) [4,9,10]
Summary
Menopause constitutes a transitional period from reproductive to non-reproductive life, which is mainly characterized by a major reduction in estrogens production and androgenicity [1]. It has been shown that androgens can have an appreciable effect on fat distribution in PMP women, by promoting visceral abdominal fat accumulation at different stages of menopause, independently of age, race, total fat mass and other cardiovascular risk factors [15]. An increased expression and activity of enzyme 11-beta-hydroxysteroid-dehydrogenase type 1 (11βHSD1) has been documented in the adipose tissue and liver of normal-weight PMP women, leading to an increased conversion of cortisone to cortisol and excess abdominal adiposity [17] Whether all these unfavorable changes of body composition could be prevented or improved by hormone replacement treatment in PMP women, remains still unresolved [18].
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