Sex steroids enhance insulin receptors and glucose oxidation in Chang liver cells

Clin Chim Acta. 2009 Jan;399(1-2):49-53. doi: 10.1016/j.cca.2008.09.011. Epub 2008 Sep 18.

Abstract

Background: The present study was designed to assess the effect of sex steroids (testosterone and 17beta-estradiol) on insulin receptor expression, insulin binding and glucose oxidation in human liver cell line.

Methods: Non-malignant Chang liver cells were treated with different concentrations of testosterone and 17beta-estradiol dissolved in serum free medium for 24 h to identify the effective dose of both steroids for further studies. Cells with 70-80% confluency were challenged with testosterone (0.1 micromol/l), 17beta-estradiol (0.1 micromol/l) and their combination along with insulin as a positive control for 24 h. After the treatment period, insulin receptor mRNA expression, cell surface insulin binding and (14)C-glucose oxidation were assessed.

Results: Both testosterone and 17beta-estradiol significantly increased the insulin receptor mRNA expression, cell surface insulin binding and (14)C-glucose oxidation compared to basal, but the increase was not at par with the effect of insulin. Compared to individual effects of testosterone and 17beta-estradiol, their combination significantly increased the glucose oxidation similar to that of insulin.

Conclusion: It is concluded from the present study that testosterone and 17beta-estradiol can directly enhance insulin receptor mRNA expression, insulin binding and glucose oxidation in Chang liver cells and thereby glucose metabolism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Estradiol / pharmacology*
  • Gene Expression Regulation
  • Glucose / metabolism*
  • Hepatocytes / cytology
  • Hepatocytes / metabolism*
  • Humans
  • Oxidation-Reduction
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptor, Insulin / metabolism*
  • Testosterone / pharmacology*

Substances

  • RNA, Messenger
  • Testosterone
  • Estradiol
  • Receptor, Insulin
  • Glucose