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Two groups of normal male subjects were given an infusion of insulin and an infusion of epinephrine + insulin respectively. Blood glucose, plasma free fatty acids (FFA), insulin, growth hormone, cortisol, and urinary catecholamines were determined. Continuous indirect calorimetry was used to measure metabolic rate and oxidation rates of carbohydrate and lipids. The first group (n equals 7) received a 30-minute insulin infusion (0.1 IU/kg). While blood glucose and plasma FFA decreased, carbohydrate oxidation and metabolic rate significantly increased after some delay, whereas lipid oxidation decreased. The increase in carbohydrate oxidation amounted to 5 g/120 min. The decrease in blood glucose during insulin administration did not correlate with the increase in carbohydrate oxidation. In the second group (n equals 7), a 150-minute epinephrine infusion (900 mug in 500 ml saline) was administered, and superimposed upon it, a similar insulin infusion initiated after 60 min. Epinephrine alone increased blood glucose and plasma FFA levels, and decreased insulinemia. The rise in the metabolic rate was sharp and significant. After a short but significant increase the oxidation rate of carbohydrate decreased, whereas that of lipids markedly rose. This increase significantly correlated with that in FFA. Addition of insulin markedly decreased the elevated FFA levels and lowered blood glucose. After some delay this was followed by a marked increase in carbohydrate oxidation and a decrease in lipid oxidation. In this test the total increase in carbohydrate oxidation was 11 g/120 min. In comparison with the insulin test, this double amount seems to correlate well with the higher blood glucose levels measured before insulin administration. The results suggest that insulin indirectly stimulates carbohydrate oxidation by facilitating glucose transport into the cells and lowering FFA levels, and that epinephrine favours lipid oxidation through its lipolytic effects and its suppression of insulin release.

Oral tolerance tests with 30 and 50 g of xylitol were performed in 10 normal subjects adapted to taking this pentitol. A 50 g oral glucose tolerance test served as control. Continuous indirect calorimetry was carried out in 7 of these subjects to measure the effects on the metabolic rate and on the oxidation rates of carbohydrate and fat. A small and short rise in serum xylitol and low quantitites of xylitol excretion in urine were observed in both xylitol tests. Xylitol caused a small but statistically significant increase in blood glucose and plasma insulin concentrations. Plasma free glycerol diminished significantly. After xylitol the metabolic rate rose throughout the test period but the total increase was only half of that after glucose administration. There was no significant influence of xylitol on the oxidation rates of carbohydrate and lipids. The total increase in carbohydrate oxidation during 2 1/2 hours amounted to one fourth of that caused by glucose. It is suggested that xylitol, during the first two hours after ingestion, charges the body's metabolism much less than equal amounts of glucose. Therefore, the use of xylitol as a sweetener in the diet of diabetic patients seems to be justified.