Nutritional and metabolic consequences of basal hyperinsulinemia in alcoholic liver cirrhosis: relationship with postprandial changes in erythrocyte insulin-receptor affinity
Campillo, B.; Sommer, F.; Bories, P.N.; Wirquin, E.; Devanlay, M.; Pornin, B.; Fouet, P.
Nutrition 10(6): 532-537
1994
ISSN/ISBN: 0899-9007 PMID: 7703600 Document Number: 436821
The nutritional and metabolic consequences of basal hyperinsulinemia were investigated in a group of 13 alcoholic cirrhotic patients; 7 healthy subjects were studied as a control group. Two groups of patients were defined on the basis of fasting insulin level: group 1 (n = 7) displayed acute hyperinsulinemia (> mean of control group + 2SD), and group 2 (n = 6) had lower insulin levels. Nutrition status was assessed by means of anthropometric parameters; the rates of nutrient oxidation were measured after an overnight fast and 2 h after a standard meal intake. Group 1 had better nutrition status in terms of fat mass than group 2 (p < 0.05). Although the basal rates of nutrient oxidation were in the same range in the three groups, postprandially, the rate of lipid oxidation was significantly different (p < 0.01). Moreover, group 1 showed greater inhibition of postprandial lipid oxidation than the control group (p < 0.05), whereas there was no difference between group 2 and the control group. In the postprandial phase, erythrocyte insulin-receptor binding and affinity increased paradoxically in group 1, whereas they decreased in group 2 and healthy subjects (changes in binding, p < 0.025; changes in affinity, p < 0.01). In conclusion, basal hyperinsulinemia in alcoholic liver cirrhosis is related to more marked inhibition of postprandial lipid oxidation and better-preserved nutrition status and may lead to a paradoxical postprandial increase in insulin-receptor affinity.