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Glucoregulatory Function of Thyroid Hormones: Interaction with Insulin Depends on the Prevailing Glucose Concentration^*

Abt. Klinische Endokrinologie Medizinische Hochschule Hannover 3000 Hannover 61, West Germany

Address requests for reprints to: M. J. Muller, Medizinische Hochs-chule Hannover, Abt. Klinische Endokrinologie, Konstanty-Gutschow-Str.8,3000 Hannover 61, West Germany.

The effect of elevated serum thyroid hormone concentrations on insulin-induced glucose metabolism was studied in healthy subjects before and after T₄ administration (250 µg T₄/day for 10-14 days). This treatment induced moderate hyperthyroidism (T₄, 15.2 µg/dl; T₃) 200 ng/dl). The following results were obtained. Insulin receptor binding to a 90% enriched monocyte fraction or to mitogen-stimulated cultured T lymphocytes was decreased by T₄ administration, whereas insulin binding to erythrocytes was unaffected. Despite down-regulation of cellular insulin receptors, T₄ administration did not alter oral glucose tolerance, but increased the dinsappearance of glucose after an iv load and the amount of glucose metabolized during euglycemic clamp studies infusing 1.0 or 1.5 mU insulin/kg BW·min; no effect was found at insulin infusion rates of 0.5, 2.0, and 4.0 mU/kg·min. Atincreasing steady state plasma glucose levels (up to 175 mg/dl) and an insulin infusion rate of 1.0 mU/kg BW·min, T₄ administration reduced insulin-induced glucose metabolism.We conclude that experimental hyperthyroidism decreases insulin receptor binding but increases insulin-induced glucose metabolism during euglycemia. This may be due to the direct effect of thyroid hormones on glucose metabolism; however, during hyperglycemia, thyroid hormone induced insulin resistance is unequivocal.

^* This work was supported by Deutsche Forschungsgemeinschaft (Grant Mu 714/1-1) and a generous gift from Hoechst AG (Frankfurt, West Germany).

Received October 8, 1985.