Time Course of the Starve-refeed Response in Rats; the Possible Role of Insulin

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Abstract
Specific pathogen-free male Wistar rats (125 to 150 g) were subjected to several types of starvation-refeeding regimens. The activities of hepatic glucose-6-phosphate dehydrogenase and malic enzyme were decreased by starvation. When starved animals were refed a high carbohydrate diet, the activities of liver glucose-6-phosphate dehydrogenase and malic enzyme rose above ad libitum-fed values within 2 days, reached a maximum after approximately 3 days and returned almost to normal 1 week after refeeding. The time course of change of total liver lipid was similar. Serum immunoreactive insulin levels increased within 1 hour after rats were given food. The largest increases were observed at 12 and 36 hours after refeeding. Both the 12-hour and 36-hour increases were abolished by 8-azaguanine. In rats treated with azaguanine, glucose-6-phosphate dehydrogenase and malic enzyme activities returned to ad libitum-fed levels, but the overshoot was absent. Injection of protamine-zinc insulin to rats refed a high carbohydrate, adequate protein diet, and treated with azaguanine restored the malic enzyme overshoot, but not the glucose-6-phosphate dehydrogenase overshoot. Refeeding a high protein, carbohydrate-free diet restored the activities of glucose-6-phosphate dehydrogenase and malic enzyme to the prestarvation level; when the protein-refed rats were fed the high carbohydrate diet the overshoot was again noted with both enzymes. Treatment of these rats with 8-azaguanine only during the feeding of the high carbohydrate diet prevented the overshoot of glucose-6-phosphate dehydrogenase but not of malic enzyme. Inclusion of tolbutamide or ip injection of protamine-zinc insulin had no effect on hepatic glucose-6-phosphate dehydrogenase when the high protein diet was refed, although these treatments caused a small increase in malic enzyme activity. The results suggest that the control of malic enzyme synthesis may be regulated by insulin and is dependent on dietary carbohydrate. The control of glucose-6-phosphate dehydrogenase, on the other hand, may be subject to more complex regulation involving factors other than, or in addition to insulin.