Subcutaneous obesity is not associated with sympathetic neural activation

Abstract

We tested the hypothesis that muscle sympathetic nerve activity (MSNA) would not differ in subcutaneously obese (SUBOB) and nonobese (NO) men with similar levels of abdominal visceral fat despite higher plasma leptin concentrations in the former. We further hypothesized that abdominal visceral fat would be the strongest body composition- or regional fat distribution-related correlate of MSNA among these individuals. To accomplish this, we measured MSNA (via microneurography), body composition (via dual-energy X-ray absorptiometry), and abdominal fat distribution (via computed tomography) in 15 NO (body mass index </= 25 kg/m(2); 22.4 +/- 1.4 yr) and 9 SUBOB (25 </= body mass index </= 35 kg/m(2); 23.4 +/- 2.1 yr) sedentary men. As expected, body mass (94 +/- 4 vs. 71 +/- 2 kg), total fat mass (25 +/- 2 vs. 12 +/- 1 kg), and abdominal subcutaneous fat (307 +/- 36 vs. 132 +/- 12 cm(2)) were significantly higher in the SUBOB group compared with NO peers. However, the level of abdominal visceral fat did not differ significantly in the two groups (69 +/- 7 vs. 55 +/- 5 cm(2)). MSNA was not different between SUBOB and NO men (23 +/- 3 vs. 24 +/- 2 bursts/min; P > 0.05, respectively) despite approximately 2.6-fold higher (P < 0.05) plasma leptin concentration in the SUBOB men. Furthermore, abdominal visceral fat was the only body composition- or regional fat distribution-related correlate (r = 0.45; P < 0.05) of MSNA in the pooled sample. In addition, abdominal visceral fat was related to MSNA in NO (r = 0.58; P = 0.0239) but not SUBOB (r = 0.39; P = 0.3027) men. Taken together with our previous observations, our findings suggest that the relation between obesity and MSNA is phenotype dependent. The relation between abdominal visceral fat and MSNA was evident in NO but not in SUBOB men and at levels of abdominal visceral fat below the level typically associated with elevated cardiovascular and metabolic disease risk. Our observations do not support an obvious role for leptin in contributing to sympathetic neural activation in human obesity and, in turn, are inconsistent with the concept of selective leptin resistance.