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.

Sympathetic Overdrive and Cardiovascular Risk in the Metabolic Syndrome

“…The results clearly indicate that the degree of sympathetic activation (and the magnitude of the insulin resistance state) is much greater in patients with visceral body fat deposits than in those with peripheral distribution of the adipose tissue. This finding (which, as discussed below, underscores once again the close relationships between sympathetic overactivity and insulin sensitivity) has been further confirmed by the results of a study showing that subcutaneous body fat accumulation is not linked to an adrenergic overdrive (21).…”

The effect of gender on the sympathetic nerve hyperactivity of essential hypertension

“…Secondly, leptin has been proposed to activate the sympathetic nervous system in animals, 44 although in humans, the levels of plasma leptin have been reported to be related to heart rate in men only and in general to obesity but not to sympathetic nerve activity. 45,46 However, the four groups of the present study had similar BMI, waist circumference and heart rate. Thirdly, there are obvious differences in the plasma levels of sex hormones between women and men, and these have been tested in relation to MSNA.…”

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

“…Therefore, altered cytokine production may underlie the strong association between visceral fat and sympathetic activation. However, some studies have shown that leptin is more related to total or subcutaneous fat rather than to visceral fat (32,34). If this is true, direct stimulation of the central nervous system by leptin could not explain our finding that visceral fat is strongest associated with sympathetic activation.…”

“…Two of these papers also investigated SAT and reported that VAT was stronger associated with sympathetic activation than SAT (32,33). Another study reported that sympathetic activation in individuals with high subcutaneous fat was not different from nonobese individuals (34). We were able to extend these observations by showing that VAT was also associated with measures of sympathetic activation on the ECG (HR, QTc, and the ventricular gradient) after adjustment for SAT, while the association of SAT with these measures attenuated after adjustment for VAT.…”