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Glucose-6-phosphatase Activity in Copper-Deficient Rats
W Thomas Johnson1, R C Nordlie, L M Levay
1United States Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center and Department of Biochemistry and Molecular Biology, University of North Dakota School of Medicine, 58202, Grand Forks, North Dakota.
Biological Trace Element Research
|November 23, 2013
Summary
Copper deficiency reduces key glucose-6-phosphatase activities in rats. However, a decrease in enzyme latency compensates, maintaining glucose homeostasis and suggesting copper deficiency doesn't alter overall glucose metabolism.
Area of Science:
- Biochemistry
- Nutritional Science
- Metabolic Regulation
Background:
- Copper deficiency is linked to glucose intolerance.
- Hepatic glucose-6-phosphatase is crucial for glucose homeostasis.
- The enzyme's activity can be modulated by its complex structure.
Purpose of the Study:
- To investigate the impact of copper deficiency on hepatic glucose-6-phosphatase activity in rats.
- To determine if altered enzyme activity contributes to glucose intolerance.
Main Methods:
- Copper deficiency was induced in rats.
- Activities of glucose-6-P phosphohydrolase and carbamyl-P:glucose phosphotransferase were measured.
- Enzyme latency was assessed in deoxycholate-treated and untreated homogenates.
Main Results:
- Copper-deficient rats showed significantly lower total glucose-6-P phosphohydrolase and carbamyl-P:glucose phosphotransferase activities.
- Latency of both enzyme activities was reduced in copper-deficient rats.
- The decrease in latency appeared to compensate for reduced total activity.
Conclusions:
- Copper deficiency reduces the catalytic activity of hepatic glucose-6-phosphatase.
- Compensatory changes in enzyme latency suggest a functional increase in translocase activity.
- It is unlikely that copper deficiency affects glucose homeostasis in vivo solely through alterations in glucose-6-phosphatase activity.
