Body Weight, Body Fat Distribution, and Hormonal Replacement Therapy in Early Postmenopausal Women

Abstract

Body weight was measured, and body fat distribution was determined by dual energy x-ray in early postmenopausal women given either oral calcium (500 mg/day; control group; n ϭ 12) or hormonal replacement therapy (HRT), a combination of estradiol valerate (2 mg/day for 21 days) with cyproterone acetate (1 mg/day in the last 10 days of the treatment cycle; n ϭ 15). There were no differences in basal body weight or body fat distribution in the two groups before the study. In the control group, a significant (P Ͻ 0.05) increase in body weight (from 61.8 Ϯ 2.1 to 63.3 Ϯ 1.9 kg after 12 months) paralleled a slight, but significant (P Ͻ 0.05), increase in total body fat mass (from 23.8 Ϯ 2.2 to 24.7 Ϯ 2.2 kg), with an increase in fat in the trunk (from 10.2 Ϯ 0.4 to 11.3 Ϯ 0.4 kg; P Ͻ 0.01) and arms (from 2.4 Ϯ 0.5 to 2.7 Ϯ 0.2 kg; P Ͻ 0.05). These findings demonstrate a shift to a prevalent central android fat distribution after 12 months of observation in untreated postmenopausal women. Conversely, in the HRT group, total body bone mineral showed a significant (from 1089 Ϯ 28 to 1106 Ϯ 29 mg/cm 2 ; P Ͻ 0.05) increase after 12 months, with no significant increase in body weight (from 62.2 Ϯ 1.6 to 62.7 Ϯ 1.6 kg), and no modifications in trunk (from 10.0 Ϯ 0.2 to 9.8 Ϯ 0.3 kg) and arm (from 2.43 Ϯ 0.2 to 2.5 Ϯ 0.1 kg) fat, but a significant increase in leg fat (from 7.1 Ϯ 0.3 to 8.3 Ϯ 0.4 kg; P Ͻ 0.05). The present results suggest that HRT can counteract at least in part the postmenopausal increase in body weight and body fat and prevent central body fat distribution after menopause. (J Clin Endocrinol Metab 82: 414 -417, 1997)

Aromatase-deficient (ArKO) mice have a phenotype of increased adiposity

“…This phenotype is associated with a greater risk of insulinresistant diabetes, cardiovascular disease, and breast cancer (1). Estrogen insufficiency is thought to be largely responsible for the increase in adiposity during menopause because postmenopausal women who receive estrogen replacement therapy do not display the characteristic abdominal weight gain pattern usually associated with menopause (2). The role that estrogens play in lipid metabolism in the body is also highlighted by the fact that individuals of both sexes with natural mutations of the gene encoding aromatase, the enzyme responsible for estrogen biosynthesis, develop truncal obesity, insulin resistance, hypercholesterolemia, and hypertriglyceridemia (3)(4)(5)(6).…”

Menopause, estrogens, progestins, or their combination on body weight and anthropometric measures

“…Modifications linked to menopause are believed to be the consequence of gonadal steroid deficiency and counteracted by gonadal steroid supplementation. However, the effects exerted by steroid administration on body weight or fat distribution are rather conflicting (10,12,13,(15)(16)(17)(18)(19)(20), inefficacy of steroid being reported by several investigators (12,13,15,16). Inconsistencies may derive from differences in experimental design, selected population, type of menopause considered, and hormones administered.…”

Hormone Replacement Therapy, Insulin Sensitivity, and Abdominal Obesity in Postmenopausal Women

“…The menopause transition, as well as the early postmenopausal period, is associated with an increase in total and central obesity (7)(8)(9). Increased visceral fat is associated with insulin resistance (10), and this preferential storage of abdominal fat may contribute to cardiovascular disease and diabetes in postmenopausal women.…”

“…Increased visceral fat is associated with insulin resistance (10), and this preferential storage of abdominal fat may contribute to cardiovascular disease and diabetes in postmenopausal women. Estrogen and HRT may improve fat distribution in postmenopausal women by preventing the increase in central body fat (7,(11)(12)(13). However, the evidence concerning the effects of HRT on glucose homeostasis is controversial.…”