| Abstract: | Excessive alcohol ingestion disturbs the metabolism of most nutrients. Although alcohol can lead to severe hypoglycemia, alcoholics are usually glucose intolerant, probably due to a inhibition of glucose-stimulated insulin secretion. Ethanol intake also leads to negative nitrogen balance and an increased protein turnover. Alcohol also alters lipid metabolism, causing a profound inhibition of lipolysis. Looking for an association between alcohol intake, nutrition, and alcoholic liver disease, we have observed a higher prevalence of subclinical histologic liver damage among obese alcoholics. Multivariate analysis in a large group of alcoholics has shown that obesity is an independent predictor of alcoholic liver disease. Other authors have reported that alcoholics with a history of obesity have a two to three times higher risk of having alcoholic liver disease than non-obese alcoholics. The possible explanation for this association is that the microsomal system, which plays an important pathogenic role in alcoholic liver disease, is induced in non-alcoholic obese subjects and alcoholics. Also, peripheral blood monocyte cells of obese alcoholics produce higher levels of interleukin-1, a cytokine that can contribute to liver damage. The ingestion of polyunsaturated fatty acids can also increase the damaging effects of alcohol on the liver, as has been demonstrated in rats subjected to continuous intragastric infusion of alcohol. Observations in human alcoholics have shown that liver damage is associated with a higher ratio of C:18:1/C:18:0 and a lower ratio of C:22:4/C:18:2 in liver lipids, consistent with an induction of delta 9 desaturase and an increased peroxidation of C:22:4. |
