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pubmed-article:8626617pubmed:abstractTextOverproduction 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.lld:pubmed
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pubmed-article:8626617pubmed:dateRevised2011-11-17lld:pubmed
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pubmed-article:8626617pubmed:articleTitleGlucose regulates in vivo glucose-6-phosphatase gene expression in the liver of diabetic rats.lld:pubmed
pubmed-article:8626617pubmed:affiliationDiabetes Research and Training Center and Division of Endocrinology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.lld:pubmed
pubmed-article:8626617pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8626617pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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