Ethanol Ingestion and Incorporation of 32P into Phospholipids of Pancreas in the Rat

Abstract

The incorporation of 32P into pancreas phospholipids was studied in the following groups of rats: (a) normal; (b) chronic ethanol ingestion (4.8 g per kg of body weight for 75 days) ; (c) acute ethanol ingestion (4.8 g per kg of body weight in two doses); (d) chronic glucose administration by intragastric tube in amounts isocaloric with the amount of ethanol given in group b; (e) chronic saline administration by intragastric tube (1.5 ml daily for 75 days) ; (f) vagotomized; and (g) sham-operated. The effect of stimulation with β-methylcholine was investigated (1.25 mg administered subcutaneously) in normal control rats, in rats under chronic ethanol ingestion, and in vagotomized rats. Rats under acute or chronic ethanol ingestion have significantly lower incorporation of 32P into pancreas phospholipids than controls and rats in which ethanol had been replaced by isocaloric amounts of glucose. This difference is abolished in the group with chronic ethanol ingestion by the administration of f3-methylcholine. The same dose of β-methylcholine has no effect on 32P incorporation in normal rats. Withdrawal of ethanol for 7 days in the group with acute ethanol ingestion returns the labeling of pancreas phospholipids to normal levels; on the other hand, in the group with chronic ethanol ingestion, only after 27 days of ethanol withdrawal was there a significant increase in 32P incorporation, but without reaching normal values. Vagotomy reduces the incorporation of 32P into pancreas phospholipids in the rat. This effect is not shown in sham-operated animals. After β-methylcholine administration, there is a significant increase in 32P incorporation, but the values are still significantly below normal levels. The possibility of ethanol interfering with a cholinergic mechanism, necessary for normal 32P incorporation into pancreas phospholipids, is discussed.