| Abstract: | Objective: To test the hypothesis that the greater β‐adrenoceptor (β‐AR)‐stimulated lipolysis and sensitivity (half‐maximal lipolytic response) in abdominal (ABD) adipocytes, greater gluteal (GLT) adipose tissue‐lipoprotein lipase (AT‐LPL) activity, and dyslipidemia associated with obesity in older women are modifiable by weight loss (WL) and are not due to menopause or aging. Research Methods and Procedures: The metabolic effects of 6 months of hypocaloric diet and low‐intensity walking WL program on the regional regulation of in vitro lipolysis and AT‐LPL activity in subcutaneous ABD and GLT adipocytes were measured in 34 obese (48.7 ± 0.7% body fat, mean ± SE) postmenopausal (59 ± 1 years) white women. Results: The lipolytic responsiveness to the β‐AR agonist isoproterenol and basal lipolysis in the presence of 1 U/mL adenosine deaminase‐uninhibited (lipolysis) were greater (p < 0.01) in ABD than GLT adipocytes before and after WL, but there were no regional differences in postreceptor (dibutyryl 3′, 5′‐cyclic adenosine monophosphate)‐stimulated lipolysis. β‐AR sensitivity was greater in ABD than GLT adipocytes before (p < 0.01) but not after WL. Regional AT‐LPL did not change after WL, but the change in the activity of ABD (but not GLT) AT‐LPL correlated with the baseline adenosine deaminase‐uninhibited lipolysis (r = 0.38, p = 0.03). There were no relationships between the declines in plasma triglyceride or increases in high‐density lipoprotein cholesterol associated with WL and the changes in regional fat cell metabolism. Discussion: Thus, despite improving lipoprotein lipid profiles in obese, postmenopausal women, WL does not affect the regulation of regional fat metabolism, and a greater tonic inhibition of basal lipolysis by endogenous adenosine may increase the activity of AT‐LPL after WL and predispose older women to develop ABD adiposity. |
