Circulating visfatin level and visfatin/insulin ratio in obese women with metabolic syndrome

نویسندگان

  • Magdalena Olszanecka-Glinianowicz
  • Piotr Kocełak
  • Marcin Nylec
  • Jerzy Chudek
  • Barbara Zahorska-Markiewicz
چکیده

INTRODUCTION Visfatin is an adipokine secreted by visceral adipose tissue with insulin-mimetic properties. Higher circulating visfatin levels were reported in type 2 diabetes. The aim of this study was to analyse circulating visfatin and insulin levels and the visfatin/insulin ratio in obese women with and without metabolic syndrome (MetS). MATERIAL AND METHODS The study involved 92 obese women. Subjects were diagnosed with MetS according to IDF 2005 criteria. The MetS group consisted of 71 subjects (age: 52.8 ±9.4 years, body mass index [BMI]: 39.1 ±5.6 kg/m(2), waist circumference: 109.6 ±11.4 cm and fat mass: 52.0 ±12.8 kg) while the non-MetS group consisted of 21 subjects (age: 51.7 ±9.5 years, BMI: 36.3 ±5.2 kg/m(2), waist circumference: 104.7 ±11.0 cm and fat mass: 45.2 ±10.7 kg). In addition to anthropometric measurements and assessment of serum glucose and lipids, plasma concentrations of visfatin were estimated by enzyme-linked immunosorbent assay (ELISA) and of insulin by radioimmunoassay (RIA). Homeostatic model assessment insulin resistance (HOMA-IR) and visfatin/insulin ratio were calculated. RESULTS In the MetS group significantly higher (p < 0.01) plasma concentrations of insulin and HOMA-IR values but similar visfatin levels were observed than in the non-MetS group. As a consequence of the significantly higher plasma insulin concentration the visfatin/insulin ratio was significantly lower in the MetS group (p < 0.05). The visfatin/insulin ratio correlated inversely with anthropometric parameters such as body mass, BMI, body fat and waist circumference (r = -0.41, p = 0.0003; r = -0.42, p = 0.0002; r = -0.29, p = 0.01; r = -0.23, p = 0.04, respectively). CONCLUSIONS We conclude that the visfatin/insulin ratio declining with increasing visceral obesity may predispose to the development of insulin resistance.

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عنوان ژورنال:

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2012