CARBOHYDRATE METABOLISM IN ADDISON'S DISEASE 1

Abstract

The rate of intraven. inj. of 20% glucose soln. was adjusted to infuse 0.5 gm. glucose/kg. in 30 min., thus approximating the rate of intestinal absorption. Capillary blood sugar detns. were detd. in the fasting state and at 30-min. intervals for 4 hrs. following the glucose infusion. Urine was collected at appropriate intervals and analyzed for sugar. In most of the patients with Addison''s disease the observed abnormalities in carbohydrate metabolism included a low-normal fasting blood glucose, a marked hypoglycemia during fasting, as well as after glucose infusion, during fever or infections and on a diet high in fat and low in carbohydrate; hypoglycemic symptoms appeared at lower threshold, the tolerance curve was flat and without rebound after intraven. glucose and the response to epinephrin was decreased; the high R. Q. was excessively increased over normal after glucose adm., and B. M. R. was low-normal. Except for the oral glucose tolerance curve, desoxycorticosterone acetate did not significantly alter these abnormalities. Treatment with large quantities of adrenal cortical extract (Wilson, 50 cc), 17-hydroxy-ll-dehydrocorticosterone (Compound E, Kendall, 33 mgm.), and corticosterone (85 mg.), in order of potency, increased the fasting blood glucose level, decreased the R. Q., increased the blood glucose level and renal excretion of N, decreased the R. Q. after an intraven. tolerance test, increased the threshold of hypoglycemic symptoms, and increased the B. M. R. Such treatment also increased the glycemic response to epinephrin and the fasting blood glucose level during fever and infections. The adrenal cortical hormone thus has a direct action on carbohydrate metabolism in man as well as in animals. These data suggest that it increases the ability of the organism to form glucose and glycogen from intermediate products of both carbohydrate and protein metabolism and thus regulates the utilization of carbohydrate.