Alcoholic hypoglycemia as a result of acute challenges of ethanol

Abstract

Results from three experiments indicate that severing the subdiaphragmatic vagus in rats increased the rate of extinction of learned taste aversions. In Experiment 1, although vagotomized rats acquired a saccharin aversion equivalent to that of controls when the illness-inducing agent was the blood-borne toxin apomorphine, vagotomized rats tended to consume more saccharin than controls during repeated extinction tests. In Experiment 2, vagotomy disrupted retention and increased extinction of a preoperatively acquired saccharin aversion. Disruptions were found when the taste aversion was induced by copper sulfate, a local gastric irritant (Experiment 2A), or apomorphine, a systemic toxin (Experiment 2B); in each experiment vagotomized rats consumed more saccharin than controls on the first retention test and extinguished the prior to surgery. Experiment 3 demonstrated that vagotomy did not affect retention or extinction of a shock-induced conditioned emotional response (lick to suppression) to noise. It is concluded that integrity of the vagus is not necessary for acquisition of a learned taste aversion when a blood-borne toxin is used as the ill-inducing agent. However, the vagus apparently mediates an integral portion of the conditioned response following taste-illness acquisition regardless of whether the illness agent is a local gastric irritant or a systemic toxin.

Similar metabolic response to acute ethanol intake in pregnant and non-pregnant rats either fed or fasted

“…In the fasting state, ethanol intake produced hypoglycemia. Our present findings in virgin animals coincide with previous reports (Potter and Morris, 1980;Tramil et al, 1981) and a similar response was found to occur in fasted pregnant rats. In the fasted state, blood glucose levels depend on glucose synthesis which is known to be enhanced in virgin and pregnant animals (Herrera et al, 1969).…”