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.
Parthasarathy
Chandrakesan
C
Department of Endocrinology, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600 113, Tamil Nadu, India.
Renuka
Venkatraman Natarajan
VN
Balasubramanian
Karundevi
K
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