This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Excess abdominal visceral fat is associated with increased risk for coronary artery disease (CAD), Type 2 diabetes mellitus (DM), and hypertension. Although premenopausal women are largely protected against abdominal obesity, visceral fat accumulation increases after the menopause and there are concomitant deleterious changes in risk factors for CAD and Type 2 DM. Estrogen replacement attenuates increases in body weight and waist girth in postmenopausal women. However, it is not known whether estrogen use prevents or diminishes the visceral fat accumulation that occurs after menopause. It is possible that protective effects of estrogens on visceral fat metabolism contribute to the purported cardioprotective actions of estrogens.
The specific aims of the proposed studies are to determine in postmenopausal women whether: (1) estrogen use augments reductions in visceral fat; (2) estrogen use attenuates increases in visceral fat; and (3) changes in visceral adiposity are associated with changes in certain risk factors for CAD and Type 2 DM independent of and in addition to the effects of estrogens. An additional aim is to determine whether raloxifene exerts similar effects as estrogens on visceral fat metabolism. Raloxifene is a popular selective estrogen receptor modulator (SERM) that is being promoted as a safer alternative to estrogen not only for its protection against osteoporosis but also for possible cardioprotective effects. To meet these aims, 118 healthy but overweight postmenopausal women, aged 50-70 years, will be randomly assigned to placebo, estrogen, and raloxifene treatment groups. Reductions in visceral adiposity will be induced in all groups through a 6-month weight reduction program, involving exercise and mild dieting. Subsequent increases in adiposity will be measured through a 12-month follow-up period during which time the hormone/drug treatment will continue. It is hypothesized that women treated with estrogen will have larger reductions in abdominal fat during the period of weight loss and will reaccumulate less abdominal fat during the 12-month follow-up than women who receive placebo treatment. Changes in risk factors for CAD and Type 2 DM (blood lipids and lipoproteins, glucose tolerance, insulin resistance) in response to reductions and gains in visceral adiposity will also be measured.
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