Levels of telomerase catalytic subunit mRNA as a predictor of potential malignancy.

The regulation of glucose-6-phosphatase (G-6-Pase) catalytic subunit and glucose 6-phosphate (G-6- P) transporter gene expression by insulin in conscious dogs in vivo and in tissue culture cells in situ were compared. In pancreatic-clamped, euglycemic conscious dogs, a 5-h period of hypoinsulinemia led to a marked increase in hepatic G-6-Pase catalytic subunit mRNA; however, G-6 -P transporter mRNA was unchanged. In contrast, a 5-h period of hyperinsulinemia resulted in a suppression of both G-6-Pase catalytic subunit and G-6 -P transporter gene expression. Similarly, insulin suppressed G-6-Pase catalytic subunit and G-6 -P transporter gene expression in H4IIE hepatoma cells. However, the magnitude of the insulin effect was much greater on G-6-Pase catalytic subunit gene expression and was manifested more rapidly. Furthermore, cAMP stimulated G-6-Pase catalytic subunit expression in H4IIE cells and in primary hepatocytes but had no effect on G-6 -P transporter expression. These results suggest that the relative control strengths of the G-6-Pase catalytic subunit and G-6 -P transporter in the G-6-Pase reaction are likely to vary depending on the in vivo environment.

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Selective stimulation of G-6-Pase catalytic subunit but not G-6-Ptransporter gene expression by glucagon in vivo and cAMP in situ

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00455.2003 ◽

2004 ◽

Vol 286 (5) ◽

pp. E795-E808 ◽

Cited By ~ 18

Author(s):

Lauri A. Hornbuckle ◽

Carrie A. Everett ◽

Cyrus C. Martin ◽

Stephanie S. Gustavson ◽

Christina A. Svitek ◽

...

Keyword(s):

Gene Expression ◽

Hepg2 Cells ◽

Binding Protein ◽

Catalytic Subunit ◽

Conscious Dogs ◽

Transporter Gene ◽

Camp Response Element ◽

Subunit Mrna ◽

Enhancer Binding Protein

We recently compared the regulation of glucose-6-phosphatase (G-6-Pase) catalytic subunit and glucose 6-phosphate (G-6- P) transporter gene expression by insulin in conscious dogs in vivo (Hornbuckle LA, Edgerton DS, Ayala JE, Svitek CA, Neal DW, Cardin S, Cherrington AD, and O'Brien RM. Am J Physiol Endocrinol Metab 281: E713–E725, 2001). In pancreatic-clamped, euglycemic conscious dogs, a 5-h period of hypoinsulinemia led to a marked increase in hepatic G-6-Pase catalytic subunit mRNA; however, G-6- P transporter mRNA was unchanged. Here, we demonstrate, again using pancreatic-clamped, conscious dogs, that glucagon is a candidate for the factor responsible for this selective induction. Thus glucagon stimulated G-6-Pase catalytic subunit but not G-6- P transporter gene expression in vivo. Furthermore, cAMP stimulated endogenous G-6-Pase catalytic subunit gene expression in HepG2 cells but had no effect on G-6- P transporter gene expression. The cAMP response element (CRE) that mediates this induction was identified through transient transfection of HepG2 cells with G-6-Pase catalytic subunit-chloramphenicol acetyltransferase fusion genes. Gel retardation assays demonstrate that this CRE binds several transcription factors including CRE-binding protein and CCAAT enhancer-binding protein.

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