Abstract
The effect of insulin-induced hypoglycemia on TSH release was studied in 7 normal subjects (Group I), 5 patients with sellar enlargment, 1 patient with idiopathic panhypopituitarism (Group II-A) and 2 acromegalic patients (Group II-B). Serial measurements of TSH, GH and corrtisol, after a bolus of insulin (0.1 U/kg body weight), were made over a period of 120 min. The peak TSH value of 8.3 plus or minus 0.9 pU/ml (mean plus or minus SEM) did not differ statistically from the basal value of 6.0 plus or minus 1.3 pU/ml in Group I. GH levels, however, increased from 1.0 plus or minus 0.0 ng/ml to 28.1 plus or minus 4.3 ng/ml, which was highly significant (P less than 0.001). In contrast, Group II-A patients had an increase in serum TSH from 4.3 plus or minus 1.4 pU/ml to 28.6 plus or minus5.7 pU/ml (P less than 0.02). The peak GH levels of 4.0 plus or minus 1.7 ng/ml did not differ significantly from the basal value of 1.2 plus or minus ng/ml. In group II-B, the untreated acromegalic patient (G) did not show alterations in TSH levels consonant with the increase in GH from a basal value of 34.9 ng/ml to a peak of 46.9 ng/ml with the induction of hypoglycemia. In the treated acromegalic subject (H), basal GH increased from 7.8 ng/ml to 11.4 ng/ml with no significant changes in TSH. Serum cortisol levels in Groups I, II-A and II-B did not show consistent inverse relationship to circulating TSH. The observations in this study suggest that hypoglycemia may stimulate TSH release in certain pituitary disorders. Through GH release might play an inhibitory role on TSH secretion, the results suggest other unidentified factor(s).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: The Journal of clinical endocrinology and metabolism
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.