Abstract
The chronic metabolic effects of an increased consumption of galactose as lactose hydrolysate syrup (LHS) in man and the influence of the sex of the consumer and the menstrual cycle on peroral galactose tolerance were investigated. Chronic metabolic effects of dietary galactose were studied in rats and guinea-pigs. Inclusion of LHS in the diet of human volunteers for 10 weeks so that 6-7% of the energy intake was supplied by carbohydrate in the syrup did not increase fasting serum galactose levels or influence the tolerance of an acute peroral galactose load. Fasting serum glucose, insulin and total cholesterol levels and normal liver function were not altered. There was an increase in fasting serum triglycerides which was greater in males than females but was not of clinical importance and could not be attributed to an increased consumption of galactose as LHS per se. There was no sex difference in acute peroral galactose tolerance. Female subjects showed a consistently lower tolerance during the secretory or early pre-mentrual phase of the ovulatory menstrual cycle than during the menstrual or preovulatory phase. Differences in renal galactose excretion or in the rate of liquid gastric emptying were not involved. Consumption of diets containing 20 or 30% of the metabolisable energy as galactose for 10 weeks caused cataract development in rats but not in guinea-pigs. Fasting plasma galactose and albumin concentrations were not altered in either species. Fasting plasma glucose levels were increased in rats fed galactose at the higher level of intake. Chronic galactose consumption did not affect the hepatic or erythrocyte galactokinase activity in rats or guinea-pigs, but reduced the hepatic activity of UDP-galactose-4-epimerase in rats when fed at 20% of the metabolisable dietary energy. Changes in the activity of galactokinase or UDP-galactose-4-epimerase in the red blood cells of rats or guinea-pigs did not reflect changes in their activity in the liver. An influence of dietary galactose on water uptake and urine production was described in rats. Fasting plasma sodium and potassium levels were not altered.