Rat liver uridine diphosphate glucose dehydrogenase: dual mechanism of regulation in vivo |
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| Authors: | S M Kelkar |
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| Affiliation: | 1. Department of Endocrinology and Metabolism, Academic Medical Center, 1105AZ Amsterdam, the Netherlands;2. Department of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center, 1105AZ Amsterdam, the Netherlands;3. Department of Radiology, Academic Medical Center, 1105AZ Amsterdam, the Netherlands;4. Department of Medicine, Academic Medical Center, 1105AZ Amsterdam, the Netherlands;5. Department of Vascular Medicine, Academic Medical Center, 1105AZ Amsterdam, the Netherlands;6. Department of Internal Medicine, VU University Medical Center, 1081HV Amsterdam, the Netherlands;7. Institute for Cardiovascular Research, VU University Medical Center, 1081HV Amsterdam, the Netherlands;8. Howard Hughes Medical Institute, Yale University, New Haven, CT 06519, USA;9. Department of Medicine, Yale University School of Medicine, New Haven, CT 06520, USA;10. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA;11. Metabolism and Reward Group, Netherlands Institute for Neuroscience, 1105BA Amsterdam, the Netherlands;1. INSERM UMR 1124, Toxicologie Pharmacologie et Signalisation Cellulaire, 45 Rue des Saints-Pères, 75006 Paris, France;2. Université Paris Descartes, Sorbonne Paris Cité, 45 Rue des Saints-Pères, 75006 Paris, France |
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| Abstract: | Rat liver UDPglucose (UDPG) dehydrogenase activity was observed to be decreased after fasting and could be restored to normal levels after refeeding glucose. This could be prevented by prior injection of puromycin, suggesting de novo protein synthesis. Administration of insulin to normal rats on stock diet did not influence the enzyme activity. However, the enzyme activity was decreased in the diabetic condition. Intraperitoneal injection of insulin caused an enhancement of the enzyme activity in diabetic animals. Hepatic UDPG dehydrogenase activity was observed to be decreased on ascorbic acid feeding or intraperitoneal injection of the same. The intraperitoneal injection of either insulin or cAMP to ascorbic acid-treated rats resulted in an increase in enzyme activity reaching normal levels. The insulin-mediated increase could not be prevented by prior injection of puromycin, suggesting a post-translational effect. These results indicate two distinct mechanisms for in vivo regulation of hepatic UDPG dehydrogenase. |
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