Potential association between endogenous leptin and sympatho-vagal activities in young obese Japanese women.
Leptin is an adipocyte-derived hormone that decreases food intake and increases energy expenditure through the activation of the sympathetic nervous system (SNS). Notwithstanding recent intensive research, the underlying physiological mechanism of leptin as well as the etiology of obesity in humans remains elusive. The present study attempted to investigate the potential association between endogenous circulating leptin and sympatho-vagal activities in age- and height-matched obese and nonobese healthy young women. Plasma leptin concentrations were measured by radioimmunoassay. The autonomic nervous system activity was assessed during the resting condition by means of a recently devised power spectral analysis of heart rate variability, which serves to identify three separate frequency components, very low (VLO), low (LO), and high (HI). Plasma leptin concentrations were greater in the obese than in the control group (45.7 +/- 5.89 vs. 11.2 +/- 1.10 ng. ml(-1), P < 0.01). As to the contribution of endogenous leptin to SNS activity, both the ratios of the VLO frequency component reflecting thermoregulatory sympathetic function and the global SNS index [(VLO + LO)/HI] to plasma leptin concentration were markedly reduced in the obese compared to the control group (VLO per leptin: 5.9 +/- 1.39 vs. 37.8 +/- 8.1 ms(2). ml. ng(-1), P < 0.01; SNS index per leptin: 0.04 +/- 0.008 vs. 0.33 +/- 0.01 ml c. ng(-1), P < 0.01). Additionally, a nonlinear regression analysis revealed that these ratios exponentially decreased as a function of body fat content (VLO per leptin r(2) = 0.57, P < 0.01; SNS index per leptin r(2) = 0.53, P < 0.01). Our data suggest that reduced sympathetic responsiveness to endogenous leptin production, implying peripheral leptin resistance, might be a pathophysiological feature of obesity in otherwise healthy young women. The findings regarding the association of leptin, body fat content, and SNS activity further indicate that the 30% of total body fat, which has been used as a criterion of obesity, might be a critical point at which leptin resistance is induced.
Matsumoto
Tamaki
T
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Miyatsuji
Aya
A
Miyawaki
Takashi
T
Yanagimoto
Yukio
Y
Moritani
Toshio
T
D001823:Body Composition; D004562:Electrocardiography; D005215:Fasting; D005260:Female; D006339:Heart Rate; D006801:Humans; D020738:Leptin / Q000097:blood / Q000502:physiology*; D009765:Obesity / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*
D020738:Leptin