Eur J Endocrinol
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DOI: 10.1530/eje.0.1340563
European Journal of Endocrinology, Vol 134, Issue 5, 563-567
Copyright © 1996 by European Society of Endocrinology
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Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans: comparison with growth hormone

Mehboob A Hussain, Ole Schmitz, Jens OL Jorgensen, Jens S Christiansen, Jorgen Weeke, Christoph Schmid and E Rudolf Froesch

Hussain MA, Schmitz O, Jorgensen JOL, Christiansen JS, Weeke J, Schmid C, Froesch ER. Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans. Eur J Endocrinol 1996;134:563–7. ISSN 0804–4643

Insulin-like growth factor I (IGF-I) is considered to mediate some of the growth-promoting and metabolic effects of growth hormone (GH). Growth hormone treatment of healthy and GH-deficient subjects is accompanied by increased conversion of thyroxine (T4) to triiodothyronine (T3) in peripheral tissues. Whether these effects are mediated by IGF-I is unknown. To assess the respective roles of these hormones on thyroid hormone metabolism we have treated two groups of subjects. The first group consisted of eight healthy subjects who were treated with IGF-I 10 µg·kg–1·h–1 sc for 5 days). The second group consisted of eight subjects with combined GH and thyrotropin (TSH) deficiency due to acquired pituitary disease. They were treated with IGF-I (10 µg·kg–1·h–1 sc for 7 days), GH (2 IU m–2 sc q.i.d.) or both hormones together. The IGF-I treatment in healthy subjects led to an increase in free T3 (FT3) and a reduction in TSH levels, whereas FT4 and total T4 (TT4) levels remained unchanged. In the second group—in which all subjects were substituted with oral Lthyroxine—treatment with IGF-I led to an elevation of FT3 in the face of unchanged T4 levels. Growth hormone alone and GH plus IGF-I resulted in a more pronounced elevation in T3 level. The results suggest that IGF-I partially mediates the well-known effects of GH on peripheral conversion of T4 to T3. However, GH has more pronounced effects on thyroid hormones that apparently are not mediated by IGF-I.

ER Froesch, Division of Endocrinology and Metabolism, Department of Internal Medicine, University Hospital of Zürich, Rámistr, 100, 8091 Zürich, Switzerland




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