Smoking inhibits visceral fat accumulation in Turkish women Relation of visceral fat and body fat mass to atherogenic dysliplidemia, inflammatory markers, insulin resistance, and blood pressure


ONAT A., AYHAN E., Hergenc G., Can G. , BARLAN M. M.

METABOLISM-CLINICAL AND EXPERIMENTAL, cilt.58, ss.963-970, 2009 (SCI İndekslerine Giren Dergi)

  • Cilt numarası: 58 Konu: 7
  • Basım Tarihi: 2009
  • Doi Numarası: 10.1016/j.metabol.2009.02.029
  • Dergi Adı: METABOLISM-CLINICAL AND EXPERIMENTAL
  • Sayfa Sayısı: ss.963-970

Özet

We investigated among sexes the associations of visceral adipose tissue area (VAT) and body fat mass with smoking status, atherogenic dyslipidemia, inflammatory markers, insulin resistance, and blood pressure (BP). A random sample of the Turkish adult population consisting of 157 middle-aged men and women was evaluated cross-sectionally and partly prospectively. Although men were not influenced significantly, smoking vs never-smoking women had 4 years later a lower VAT (by 31 cm(2), P =.005). Fat mass was significantly correlated with homeostasis model, C-reactive protein, and BP in both sexes, although not with atherogenic dyslipidemia as was VAT. Compared with men, women had lower VAT (P <.01) and, because of interaction of sex and smoking (P =.06), tended to be less susceptible to accumulation of VAT per kilogram body fat mass. In linear regression models comprising 7 variables, VAT was associated ill men with systolic BP, apolipoprotein B, and C-reactive protein (each P =.04) and was associated in women with age, smoking status, and high-density lipoprotein cholesterol (each P <=. 01). Significant positive correlations of VAT were obtained with future systolic BP in either sex (P < .03). Body fat mass and visceral fat accumulation are inhibited by cigarette smoking in women. Markers of insulin resistance and inflammation are independently associated with visceral fat marginally in women but significantly in men. Visceral fat is better associated than fat mass with atherogenic dyslipidemia and, in men, with apolipoprotein B. Thus, sex interacts with the dynamics of cardiometabolic risk. (C) 2009 Elsevier Inc. All rights reserved.