Studies with New Zealand rabbits were done to determine the effect of hyperthyroidism on glucose utilization and insulin secretion. Tolerance tests were performed while the animals were euthyroid, and then repeated after the animals had been rendered hyperthyroid by daily sc sodium thyroxine administration (100 μg/kg/day). After the induction of hyperthyroidism, there was an increase in intravenous glucose disposal rate constant (KG) after glucose administration with no alteration in glucose—stimulated plasma insulin levels. Tissue sensitivity to insulin, and insulin half—life, were evaluated by iv injection of 0.15 U insulin per kg body wt. Hyperthyroidism produced an increase in the glucose disposal rate constant (KI) after insulin administration and a significant lowering of the glucose nadir indicating enhanced insulin sensitivity. A decreased insulin half-life was also noted during the hyperthyroid state (3.4 ± 0.3 min) as compared to the control state (5.6 ± 0.3 min). In vitro pancreas incubation studies were done, to more directly assess the effect of hyperthyroidism on insulin secretion. Although basal insulin secretion was similar from pancreas segments of hyperthyroid and euthyroid rabbits, glucose— Stimulated insulin secretion was greater from pancreas segments of hyperthyroid rabbits. (Endocrinology92: 1604, 1973)
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Marecek et al. (1973) studied this question.