THE EFFECT OF STREPTOZOTOCIN-INDUCED DIABETES ON THE PITUITARY-THYROID AXIS IN GOITROGEN-TREATED RATS

Abstract

ABSTRACT Studies of pituitary and thyroid function have been carried out in normal (intact) and diabetic Wistar rats. Diabetes was induced by a single streptozotocin injection (7 mg/100 g body weight). The animals were fed a low iodine diet (LID), and received a daily sc injection of either KClO4 (20 mg/100 g body weight) or propylthiouracil (PTU) (1.5 mg/100 g body weight) to induce hypothyroidism. Control groups received the same LID but supplemented with 0.8 μg I/g dry weight. In intact rats goitrogen-treatment induces an increase in thyroid weight and in plasma TSH concentration. However, the plasma TSH response to goitrogen-treatment in diabetics indicates that pituitary TSH secretion increases following a reduction in plasma PBI, but the response is less marked than in controls. The difference in plasma TSH between control and diabetic rats provides an explanation for the findings that diabetes diminishes the thyroid growth response to goitrogen-treatment. Moreover, in intact rats the low pituitary TSH content is a consequence of the increase in pituitary TSH secretion, while in the diabetics the low pituitary TSH content cannot be explained by an increase in TSH secretion. The effect of diabetes on the pituitary-thyroid axis cannot be attributed specifically to poor growth, because the changes in pituitary-thyroid function which are observed in the diabetic groups are not seen in intact rats with a growth rate similar to that of insulin deficient rats. Insulin administration to goitrogen-treated diabetic rats results in 1) an increase in the ability of the thyroid tissue to respond to its trophic hormone, 2) an increase in pituitary TSH secretion in response to the lowering of plasma PBI and, 3) an increase in thyroid growth response to goitrogen-treatment. Results are discussed in relation to the assumption that the lack of adequate insulin levels, or its metabolic defects, diminishes the full response of the thyroid to TSH, and affects the pituitary TSH secretion probably as a consequence of altered hypothalamic control of the pituitary function.