Production of Hypoglycemia by Solox and by Ethanol

Publisher Website
Google Scholar
Abstract
Previous attempts to produce hypoglycemia by administration of Solox, a denatured alcohol, failed because the experiments were terminated too soon. Repeated daily intoxication with Solox or ethanol produced hypoglycemia only after food had been refused. Fasting with daily intoxication with Solox or ethanol accelerated the onset of the hypoglycemia. The addition of thiamine did not delay or prevent Solox or ethanol hypoglycemia. Denaturants present in Solox without the ethanol did not produce hypoglycemia in larger amounts daily than Solox contains. Methyl isobutylketone proved the most acutely toxic substance in Solox. It stimulated, then depressed the central nervous system, and killed by respiratory failure. Liver damage was always associated with the hypoglycemia. Fatty metamorphosis with yacuolization and areas of focal necrosis that was more prominent in the region of the central vein was seen in the livers of all the hypoglycemic dogs. These livers were depleted of glycogen and laden with fat. It is believed that the ethanol intoxication initiates a stress reaction which is aggravated by the lack of food and an increased mobilization and deposition of fat in the liver which interferes with its nutrition and function to such a degree that it can no longer perform the necessary gluconeogenetic action to maintain the blood glucose at normal levels.