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Physiological Doses of Oral Casein Affect Hepatic Glycogen Metabolism in Normal Food-Deprived Rats^1,2,

Mary C. Gannon^*,,3 and Frank Q. Nuttall

Metabolic Research Laboratory, V.A. Medical Center ^* Departments of Food Science and Nutrition Department of Medicine, University of Minnesota, Minneapolis, MN 55417

In a previous study, administration of casein hydrolysate to food-deprived rats at a dose of 4 g/kg body wt resulted in an increase in portal plasma glucagon concentration. This was associated with an activation of phosphorylase a and a decrease in hepatic glycogen concentration. The present study was undertaken to determine whether similar results would be obtained with smaller doses. Doses of 1 and 2 g/kg body wt were administered to food-deprived rats. At a dose of 2 g/kg, portal plasma glucagon concentration was significantly elevated. This was associated with a slight increase in phosphorylase a activity (P < 0.05) and a 50% decrease in hepatic glycogen concentration (P < 0.01). At a dose of 1 g casein hydrolysate/kg body wt, changes in portal plasma glucagon concentration, phosphorylase a activity and hepatic glycogen concentration generally were not observed. Hepatic glucose, uridine diphosphoglucose, ATP and glucose-6-phosphate concentrations were unaffected by either dose of casein hydrolysate. The data indicate a dose-response relationship between casein hydrolysate administration and effects on glycogen metabolism in the liver. Protein-induced glycogenolysis is likely to occur when rats ingest a moderate amount of a pure protein meal.

KEY WORDS: • glycogenolysis • glycogen synthase • glucagon • dietary protein • rats

¹ Supported by grant no. DK 43018-01A1 from the National Institutes of Health, and Merit Review Research Funds from the Department of Veterans Affairs.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence should be addressed.

Manuscript received 23 June 1994. Revision accepted 17 October 1994.