It has been suggested that acute hyperglycemia stimulates somatostatin release from the hypothalamus, thus causing inhibition of growth hormone and thyrotropin secretion. Abnormal growth hormone secretory pattern to glucose load is characteristic of acromegaly, and it might reflect alterations in somatostatin release. We evaluated the sensitivity of serum thyrotropin response to presumed somatostatin inhibition during oral glucose tolerance test in 29 patients with active acromegaly, in 13 patients with inactive disease, and in 19 control persons suspected of impaired glucose tolerance. Both the acromegalic patients and the control subjects were euthyroid. Serum insulin, growth hormone, thyrotropin, free triiodthyronine, free thyroxine, and glucose were collected before and 30, 60, 90, and 120 min after the ingestion of 75 g glucose. While the free triiodthyronine and free thyroxine values did not change during the glucose test, the thyrotropin levels progressively and significantly declined in all groups. The basal to nadir thyrotropin ratio was higher in active acromegaly than in inactive disease and in control subjects (p < 0.01), suggesting that the glucose load inhibited thyrotropin stronger in active acromegalic patients. These data suggest that there is a possible strong somatostatin response to glucose load in acromegalic patients, which inhibits thyrotropin secretion. These data do not support the concept of decreased somatostatin drive in acromegaly.
- Acute hyperglycemia
- TSH secretion
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism