Glucose Intolerance in Hyperthyroidism: Role of Glucagon

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Abstract
The role of insulin in glucose intolerance of hyperthyroidism has been studied by several workers with conflicting results. However, the nature of glucagon secretion has never been investigated. Therefore, plasma glucose, insulin, and glucagon responses to an oral glucose load (100 g) were determined in normal subjects and hyperthyroid patients. Fasting plasma glucose was not abnormal in hyperthyroid patients. Peak values after oral glucose were attained at 30 min in both groups, but it was markedly elevated in hyperthyroid patients and the return to basal level was delayed. In hyperthyroidism, fasting plasma insulin was raised and the insulin response to oral glucose was exaggerated. Furthermore, peak insulin occurred later than in normal subjects. Basal glucagon was markedly elevated in 4 of 13 hyperthyroid patients, whereas it was unchanged in the remaining 9. In both groups, glucose ingestion resulted in the lowering of glucagon. However, the percent fall was smaller in hyperthyroid patients. Insulinogenic index, insulin area/glucose area, and insulin-glucose coefficient (cumulative insulin response/cumulative glucose response) were significantly decreased in hyperthyroid patients. All responses reverted to normal after treatment. We conclude that decreased glucagon suppression after glucose ingestion and insulin resistance, as indicated by various indices, are responsible for glucose intolerance in hyperthyroidism. Furthermore, hyperglucagonemia may play a role in some patients. These abnormalities revert to normal on attainment of the euthyroid state.