Nutritional and metabolic consequences of basal hyperinsulinemia in alcoholic liver cirrhosis: relationship with postprandial changes in erythrocyte insulin-receptor affinity.
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.
Campillo
B
B
Service d'Hépato-gastroentérologie et Rééducation digestive, Albert Chenevier Hospital, Créteil, France.
Sommer
F
F
Bories
P N
PN
Wirquin
E
E
Devanlay
M
M
Pornin
B
B
Fouet
P
P
D000328:Adult; D000886:Anthropometry; D001823:Body Composition; D002153:Calorimetry, Indirect; D004435:Eating / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D004912:Erythrocytes / Q000737:chemistry / Q000378:metabolism* / Q000648:ultrastructure; D005260:Female; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D007328:Insulin / Q000378:metabolism; D050356:Lipid Metabolism; D008104:Liver Cirrhosis, Alcoholic / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009752:Nutritional Status; D010084:Oxidation-Reduction; D011972:Receptor, Insulin / Q000032:analysis / Q000378:metabolism*
D007328:Insulin; D011972:Receptor, Insulin