Increased availability of nonesterifi ed fatty acids (FA) contributes to the metabolic dysfunction associated with obesity, including systemic insulin resistance and hyperlipidemia ( 1 ). It is well established that central or upper body obesity, independent of total body fat, is associated with elevated systemic nonesterifi ed FA turnover in premenopausal women. In vivo studies of FA fl uxes show that on a per gram basis, abdominal (Abd) subcutaneous (sc) fat is the main source of the high systemic lipolysis in upper body compared with lower body obese premenopausal women and that leg fat is less lipolytically active ( 1 ). However, microdialysis studies detect no depot difference in lipolysis in nonobese, premenopausal Abd and femoral sc adipose tissue ( 2 ). Nevertheless, both techniques reveal similar responses to the antilipolytic effect of insulin in Abd sc and lower body adipose tissues. In vitro studies also show similar basal lipolytic rates in Abd and gluteal (Glt) or femoral adipocytes of premenopausal women, but Glt adipocytes are more sensitive to insulin ( 3, 4 ). Whether this depot difference exists in postmenopausal women is not known, so this was one of the objectives of the current study.Overweight African-American (AA) women are more hyperinsulinemic and resistant to insulin's glucoregulatory actions than body fat-matched Caucasian (C) women ( 5, 6 ). Thus, it is logical to postulate that AAs may also exhibit higher rates of lipolysis and resistance to the antilipolytic effect of insulin. However, results in the literature on this topic are inconsistent. In premenopausal women, Abstract High fatty acid (FA) fl ux is associated with systemic insulin resistance, and African-American (AA) women tend to be more insulin resistant. We assessed possible depot and race difference in the antilipolytic effect of insulin in adipocytes isolated from abdominal (Abd) and gluteal (Glt) subcutaneous (sc) adipose tissue of overweight, postmenopausal AA and Caucasian (C) women. Percent body fat, fasting insulin, visceral adiposity, and adipocyte size was higher in AA women. Disinhibited lipolysis (presence of adenosine deaminase) per unit adipocyte surface area was similar in Abd and Glt and in AA and C. However, rates of 'basal' [submaximal phenylisopropyl adenosine (PIA) -suppressed] and insulin-suppressed lipolysis were higher in Abd of AA compared with C women even after adjustment for percent fat and visceral fat area. The race difference in rates of PIA-and insulin-suppressed lipolysis in AA were correlated with their hyperinsulinemia, but AA race, independent of fasting insulin, was associated with lower responsiveness (percent suppression) to submaximal insulin concentrations, although sensitivity (ED50) was not affected. Overall, these data are consistent with the hypothesis that decreased responsiveness of Abd adipocytes to antilipolytic effectors may contribute to higher FA availability and thereby to racial differences in insulin resistance. -Fried,