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


CONCLUSIONS
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.
Department of Endocrinology, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600 113, Tamil Nadu, India.
Chandrakesan
C
Parthasarathy
Venkatraman Natarajan
VN
Renuka
Karundevi
K
Balasubramanian
D002478:Cells, Cultured; D004958:Estradiol / Q000494:pharmacology*; D005786:Gene Expression Regulation; D005947:Glucose / Q000378:metabolism*; D022781:Hepatocytes / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D010084:Oxidation-Reduction; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism*; D013739:Testosterone / Q000494:pharmacology*
D012333:RNA, Messenger; D013739:Testosterone; D004958:Estradiol; D011972:Receptor, Insulin; D005947:Glucose