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Lowering of T3 and rise in reverse T3 induced by hyperglucagonemia: altered thyroid hormone metabolism, not altered release of thyroid hormones.
Horm Metab Res. 1987 Oct; 19(10):486-9.HM

Abstract

Recently we reported that hyperglucagonemia induced by glucagon infusion causes a decline in serum T3 and a rise in reverse T3 in euthyroid healthy volunteers. These changes in T3 and rT3 levels were attributed to altered T4 metabolism in peripheral tissues. However, the contribution of altered release of thyroid hormones by the thyroid gland could not be excluded. Since the release of thyroid hormones is inhibited in primary hypothyroidism and is almost totally suppressed following L-thyroxine replacement therapy, we studied thyroid hormone levels for up to 6 hours after intravenous administration of glucagon in subjects with primary hypothyroidism who were rendered euthyroid by appropriate L-thyroxine replacement therapy for several years. A control study was conducted using normal saline infusion. Plasma glucose rose promptly following glucagon administration demonstrating its physiologic effect. Serum T4, Free T4, and T3 resin uptake were not altered during both studies. Glucagon infusion induced a significant decline in serum T3 (P less than 0.05) and a marked rise in rT3 (P less than 0.05) whereas saline administration caused no alterations in T3 or rT3 levels. Thus the changes in T3 and rT3 were significantly different during glucagon study when compared to saline infusion. (P less than 0.01 for both comparisons). Since, the release of thyroid hormones is suppressed by exogenous LT4 administration in these subjects; we conclude that changes in serum T3 and rT3 observed following glucagon administration reflect altered thyroid hormone metabolism in peripheral tissues and not altered release by the thyroid gland.

Authors+Show Affiliations

VA Medical Center, Medical Service, Des Moines, Iowa.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

3428867

Citation

Kabadi, U M., and B N. Premachandra. "Lowering of T3 and Rise in Reverse T3 Induced By Hyperglucagonemia: Altered Thyroid Hormone Metabolism, Not Altered Release of Thyroid Hormones." Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme, vol. 19, no. 10, 1987, pp. 486-9.
Kabadi UM, Premachandra BN. Lowering of T3 and rise in reverse T3 induced by hyperglucagonemia: altered thyroid hormone metabolism, not altered release of thyroid hormones. Horm Metab Res. 1987;19(10):486-9.
Kabadi, U. M., & Premachandra, B. N. (1987). Lowering of T3 and rise in reverse T3 induced by hyperglucagonemia: altered thyroid hormone metabolism, not altered release of thyroid hormones. Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme, 19(10), 486-9.
Kabadi UM, Premachandra BN. Lowering of T3 and Rise in Reverse T3 Induced By Hyperglucagonemia: Altered Thyroid Hormone Metabolism, Not Altered Release of Thyroid Hormones. Horm Metab Res. 1987;19(10):486-9. PubMed PMID: 3428867.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lowering of T3 and rise in reverse T3 induced by hyperglucagonemia: altered thyroid hormone metabolism, not altered release of thyroid hormones. AU - Kabadi,U M, AU - Premachandra,B N, PY - 1987/10/1/pubmed PY - 1987/10/1/medline PY - 1987/10/1/entrez SP - 486 EP - 9 JF - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme JO - Horm. Metab. Res. VL - 19 IS - 10 N2 - Recently we reported that hyperglucagonemia induced by glucagon infusion causes a decline in serum T3 and a rise in reverse T3 in euthyroid healthy volunteers. These changes in T3 and rT3 levels were attributed to altered T4 metabolism in peripheral tissues. However, the contribution of altered release of thyroid hormones by the thyroid gland could not be excluded. Since the release of thyroid hormones is inhibited in primary hypothyroidism and is almost totally suppressed following L-thyroxine replacement therapy, we studied thyroid hormone levels for up to 6 hours after intravenous administration of glucagon in subjects with primary hypothyroidism who were rendered euthyroid by appropriate L-thyroxine replacement therapy for several years. A control study was conducted using normal saline infusion. Plasma glucose rose promptly following glucagon administration demonstrating its physiologic effect. Serum T4, Free T4, and T3 resin uptake were not altered during both studies. Glucagon infusion induced a significant decline in serum T3 (P less than 0.05) and a marked rise in rT3 (P less than 0.05) whereas saline administration caused no alterations in T3 or rT3 levels. Thus the changes in T3 and rT3 were significantly different during glucagon study when compared to saline infusion. (P less than 0.01 for both comparisons). Since, the release of thyroid hormones is suppressed by exogenous LT4 administration in these subjects; we conclude that changes in serum T3 and rT3 observed following glucagon administration reflect altered thyroid hormone metabolism in peripheral tissues and not altered release by the thyroid gland. SN - 0018-5043 UR - https://www.unboundmedicine.com/medline/citation/3428867/Lowering_of_T3_and_rise_in_reverse_T3_induced_by_hyperglucagonemia:_altered_thyroid_hormone_metabolism_not_altered_release_of_thyroid_hormones_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-2007-1011859 DB - PRIME DP - Unbound Medicine ER -