Regulation of lipolysis and lipoprotein lipase after weight loss in obese, postmenopausal women.

Objective: To test the hypothesis that the greater beta-adrenoceptor (beta-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 beta-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. beta-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.