Relation between insulin resistance and serum concentrations of IL-6 and TNF-alpha in overweight or obese women with early stage breast cancer


Gonullu G., Ersoy C., Ersoy A. , Evrensel T. , Basturk B., Kurt E., ...More

CYTOKINE, vol.31, no.4, pp.264-269, 2005 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 31 Issue: 4
  • Publication Date: 2005
  • Doi Number: 10.1016/j.cyto.2005.05.003
  • Title of Journal : CYTOKINE
  • Page Numbers: pp.264-269
  • Keywords: breast cancer, IL-6, insulin resistance, obesity, TNF-alpha, TUMOR-NECROSIS-FACTOR, REGULATING ESTROGEN SYNTHESIS, BETA-CELL FUNCTION, CYTOKINE RECEPTORS, HIP-RATIO, INTERLEUKIN-6, EXPRESSION, PREVENTION, ADIPOCYTE, CORRELATE

Abstract

Insulin resistance (IR) and obesity may be risk factors for breast cancer. The mechanism of IR in patients with cancer has not been fully clarified yet. This study was conducted to evaluate the possible role of circulating cytokines; tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6) in inducing IR in 20 overweight or obese patients with early stage breast cancer and to compare their levels with that of body mass index matched 20 healthy controls. IR was calculated by homeostasis model assessment (HOMA) method. Four groups were formed according to a 2.7 HOMA-IR cut-off value as breast cancer with or without IR and controls with or without IR. IL-6 and HOMA-IR values were found to be higher in breast cancer patients with IR compared to other groups. There was no significant difference in TNF-alpha levels between groups. HOMA-IR values correlated with estradiol and IL-6 levels in all breast cancer patients but not TNF-alpha. HOMA-IR values, serum insulin, estradiol and IL-6 levels in the receptor positive group were significantly higher than those of the receptor negative group. These results suggested a possible contribution of endogenous IL-6 production and hyperinsulinemia to the development of breast cancer in overweight or obese patients with prominent IR. (c) 2005 Elsevier Ltd. All rights reserved.