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1 Department of Human Nutrition, Foods and Exercise, University of Texas Health Sciences Center, Blacksburg, VA, USA
2 Virginia Polytechnic Institute and State University, Blacksburg, VA, USA
* To whom correspondence should be addressed. E-mail: kdavy{at}vt.edu.
We tested the hypothesis that muscle sympathetic nerve activity (MSNA) would not be elevated in subcutaneous obese (SUBOB) compared with 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 (microneurography), body composition (dual energy x-ray absorptiometry) and abdominal fat distribution (computed tomography) in 15 NO (body mass index 
25 kg/m2, 22.4±1.4 yrs) and 9 SUBOB (body mass index 
25 and 35 kg/m2, 23.4±2.1 yrs) 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 cm2) were significantly (all P<0.05) 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 cm2). MSNA was not different between SUBOB and NO (23±3 vs. 24±2 bursts/min, P>0.05, respectively) despite ~2.6 fold higher (P<0.05) plasma leptin concentration in the SUBOB. Furthermore, abdominal visceral fat was the only body composition- or regional fat distribution-related correlate (r=0.45, P<0.05) of MSNA in 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). Taken together with our previous observations, our findings suggest that the
relation between obesity and MSNA is phenotype dependent. In addition, the relation between abdominal visceral fat and MSNA is evident in nonobese, but not in subcutaneous obese, 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.
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