The influence of posthenopaubal hormone replacement therapy on body composition

1996 ◽  
Vol 6 (S1) ◽  
pp. 230-230
Author(s):  
W. Hänggi ◽  
K Lippuner ◽  
Ph Jaeger ◽  
MH Birkhäuser ◽  
FF Horber
2015 ◽  
Vol 18 (6) ◽  
pp. 647-661 ◽  
Author(s):  
Aileen Bahl ◽  
Eija Pöllänen ◽  
Khadeeja Ismail ◽  
Sarianna Sipilä ◽  
Tuija M. Mikkola ◽  
...  

The loss of estrogen during menopause causes changes in the female body, with wide-ranging effects on health. Estrogen-containing hormone replacement therapy (HRT) leads to a relief of typical menopausal symptoms, benefits bone and muscle health, and is associated with tissue-specific gene expression profiles. As gene expression is controlled by epigenetic factors (including DNA methylation), many of which are environmentally sensitive, it is plausible that at least part of the HRT-associated gene expression is due to changes in DNA methylation profile. We investigated genome-wide DNA methylation and gene expression patterns of white blood cells (WBCs) and their associations with body composition, including muscle and bone measures of monozygotic (MZ) female twin pairs discordant for HRT. We identified 7,855 nominally significant differentially methylated regions (DMRs) associated with 4,044 genes. Of the genes with DMRs, five (ACBA1, CCL5, FASLG, PPP2R2B, and UHRF1) were also differentially expressed. All have been previously associated with HRT or estrogenic regulation, but not with HRT-associated DNA methylation. All five genes were associated with bone mineral content (BMC), and ABCA1, FASLG, and UHRF1 were also associated with body adiposity. Our study is the first to show that HRT associates with genome-wide DNA methylation alterations in WBCs. Moreover, we show that five differentially expressed genes with DMRs associate with clinical measures, including body fat percentage, lean body mass, bone mass, and blood lipids. Our results indicate that at least part of the known beneficial HRT effects on body composition and bone mass may be regulated by DNA methylation associated alterations in gene expression in circulating WBCs.


2002 ◽  
Vol 8 (4) ◽  
pp. 137-140 ◽  
Author(s):  
Morten B Sørensen

One of the major concerns of perimenopausal women is obesity—and for a good reason. Both general and abdominal obesity as well as loss of skeletal muscle (sarcopenia) are accelerated through the menopausal transition and lifestyle changes as well as sex hormone deficiency play important roles. Most well conducted clinical trials have demonstrated hormone replacement therapy induced reversal or at least impairment of menopausal changes in body composition and the common worry that it causes weight gain is unsubstantiated. Coaching of weight loss in obese individuals is often a frustrating task but is nevertheless of immense importance because of the health hazards of obesity. Through the climacteric period, short-term hormone replacement therapy, with or without androgens for preservation of muscle mass, might inhibit obesity and this is likely to boost motivation for introduction of more comprehensive and long-lasting initiatives linked to persistent weight loss and long-term health benefit.


1999 ◽  
Vol 163 (1) ◽  
pp. 55-62 ◽  
Author(s):  
K Kristensen ◽  
SB Pedersen ◽  
P Vestergaard ◽  
L Mosekilde ◽  
B Richelsen

Leptin and oestrogen are both involved in the regulation of adipose tissue deposition and feeding behaviour. We investigated whether 5 years of hormone replacement therapy (HRT) affected serum leptin and body composition differently in 89 postmenopausal women treated with HRT compared with 178 controls. At baseline, leptin was significantly correlated with oestradiol (r=0.13, P<0.05) and in multiple backward regression analysis including oestradiol and any estimate of body fat, oestradiol remained a significant determinant of leptin levels. In the control group, all estimates of body fat determined by dual energy X-ray absorptiometry (DEXA) or anthropometry were increased (3.6-16.9%) and leptin increased 31.3% (16.03+/-1.02 to 20.84+/-1.2 ng/ml (s.e.m.), P<0.001). In the HRT group all estimates of body composition also increased during the 5-year observation but to a lesser extent than observed in the control group (1.0-8.5%). Leptin was raised by 19.7% (17.81+/-1.32 to 20.57+/-1.65 ng/ml, P<0.001). However, the DEXA scans revealed that the control group gained 2.4-fold more fat during the 5-year observation (1.9+/-0.3 vs 0.8+/-0.4 kg, P<0.05), and especially the trunk fat increased (1.4+/-0.2 vs 0.7+/-0.3 kg, P<0.05). This was reflected in the increase in leptin levels, which were increased by 7.4% in the control group compared with the HRT group (4.81+/-0.60 vs 2.76+/-0.87 ng/ml, P<0.05). Adjusting for the difference in adipose tissue revealed that HRT had no independent effect on leptin levels. Comparisons between obese (body mass index>25 kg/m(2)) and non-obese (<25 kg/m(2)) subjects by stratifying for HRT treatment using multiple linear regression revealed that the change in fat mass was significantly less among treated subjects (P=0.038) and especially in the non-obese subjects (P=0.001). The change in trunk fat was similarly correlated with treatment status (P=0.029) and with the degree of obesity (P=0.006). In conclusion, 5 years of HRT treatment significantly reduced fat mass accumulation, especially in the trunk region. This effect of HRT was more pronounced in non-obese as compared with obese subjects. The HRT-induced reduction in fat mass seems not to be mediated by leptin.


Sign in / Sign up

Export Citation Format

Share Document