Glucose regulates in vivo glucose-6-phosphatase gene expression in the liver of diabetic rats

J Biol Chem. 1996 Apr 26;271(17):9871-4. doi: 10.1074/jbc.271.17.9871.

Abstract

Overproduction of glucose by the liver is the major cause of fasting hyperglycemia in both insulin-dependent and non-insulin-dependent diabetes mellitus. The distal enzymatic step in the process of glucose output is catalyzed by the glucose-6-phosphatase complex. We show here that 90% partially pancreatectomized diabetic rats have a >5-fold increase in the messenger RNA and a 3-4-fold increase in the protein level of the catalytic subunit of glucose-6-phosphatase in the liver. Normalization of the plasma glucose concentration in diabetic rats with either insulin or the glycosuric agent phlorizin normalized the hepatic glucose-6-phosphatase messenger RNA and protein within approximately 8 h. Conversely, phlorizin failed to decrease hepatic glucose-6-phosphatase gene expression in diabetic rats when the fall in the plasma glucose concentration was prevented by glucose infusion. These data indicate that in vivo gene expression of glucose-6-phosphatase in the diabetic liver is regulated by glucose independently from insulin, and thus prolonged hyperglycemia may result in overproduction of glucose via increased expression of this protein.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental / enzymology*
  • Energy Metabolism
  • Gene Expression Regulation, Enzymologic
  • Glucose / metabolism*
  • Glucose-6-Phosphatase / metabolism*
  • Hyperglycemia / enzymology
  • Insulin / pharmacology
  • Liver / enzymology*
  • Male
  • Phlorhizin / pharmacology
  • RNA, Messenger / genetics
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Insulin
  • RNA, Messenger
  • Phlorhizin
  • Glucose-6-Phosphatase
  • Glucose