Abstract
In women there is an increase in visceral obesity, subcutaneous abdominal adipocyte lipolysis, and risk of cardiovascular disease (CVD) associated with weight gain after menopause. The mechanisms underlying this increase in adrenoreceptor (AR)-agonist catecholamine-stimulated lipolysis and abdominal obesity in postmenopausal women were studied in intact adipocytes isolated from the abdominal and gluteal subcutaneous fat depots in 19 obese (48% ± 1% body fat, mean ± SE) women with a mean ± SE age of 58 ± 1 years. The fat cell size and adipose tissue lipoprotein lipase (ATLPL) activity were similar in both sites. The maximal lipolytic responsiveness and sensitivity to isoproterenol were higher (
P < .05) in abdominal compared with gluteal adipocytes, but maximal lipolytic response to a post-AR agent was similar. Abdominal adipocytes had a higher β-AR ([
3H]-CGP-12177) and α
2-AR ([
3H]-yohimbine) affinity than gluteal cells (
P < .05), lower α
2-AR density (
P < .05), but similar β-AR density as gluteal cells. Both abdominal and gluteal cell size correlated with α
2-AR (density (
P < .01), but not with β-AR density. Thus, a higher β-AR affinity and lower α
2-AR relative to β-AR density may explain the higher in vitro catecholamine-mediated lipolysis in abdominal compared with gluteal adipocytes in obese, postmenopausal women.
