Hepatic gamma-glutamyltransferase activity: its increase following chronic alcohol consumption and the role of carbohydrates

Abstract

Prolonged feeding of diets containing ethanol leads to a significant increase of hepatic gamma-glutamyltransferase (GGT) activity which has been ascribed either to ethanol itself or to dietary imbalance with respect to carbohydrates. Hepatic GGT activity was therefore determined in Sprague-Dawley rats fed for five weeks liquid diets containing various amounts of protein, fat and vitamins. Compared to the normal control diet containing 47% of total calories as carbohydrates, a hypocaloric diet with 11% of total calories of the control diet as carbohydrates failed to result in major alterations of hepatic GGT activity (0.27 +/- 0.04 Units/g liver wet weight vs 0.35 +/- 0.06; N.S.). Similarly, hepatic GGT activity remained virtually unchanged under a hypercaloric carbohydrate rich diet. However, hepatic GGT activity was strikingly enhanced by a diet in which carbohydrates were replaced to the extent of 36% of total calories by ethanol to achieve a carbohydrate content of 11% (0.66 +/- 0.12 Units/g liver; P less than 0.005), indicating that alcohol itself is capable of increasing hepatic GGT activity. However, alcohol given with a high carbohydrate diet was shown to be incapable of increasing the hepatic activity of GGT. These data therefore indicate that upon chronic intake ethanol itself enhances hepatic GGT activity provided that the carbohydrate content of the diet is low, whereas such an effect could not be observed with ethanol in a high carbohydrate diet.