This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fragner, P. Articles by Aratan de Leon, S. Search for Related Content PubMed PubMed Citation Articles by Fragner, P. Articles by Aratan de Leon, S. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB LIOTHYRONINE

Triiodothyronine Down-Regulates Thyrotropin-Releasing Hormone (TRH) Synthesis and Decreases pTRH-(160–169) and Insulin Releases from Fetal Rat Islets in Culture¹

INSERM U-30, Mécanisme d’Action Cellulaire des Hormones, Tour Lavoisier, Hôpital Necker Enfants Malades, 75743 Paris Cedex 15; and Laboratoire de Bioactivation des Peptides, Institut Monod (A.L.), 75005 Paris Cedex 5, France

Address all correspondence and requests for reprints to: Dr. Sonia Aratan de Leon, INSERM U-30, Hôpital Necker-Enfants-Malades, 149 rue de Sèvres, 75743 Paris Cedex 15, France.

TRH is localized with insulin in ß-cells. It is synthesized as a prohormone containing five copies of TRH and seven cryptic peptides, including pro (p)-TRH-(160–169). Thyroid hormone regulates the expression of several genes encoding peptide hormones. We found that circulating T₃ concentrations were inversely correlated with TRH levels in two physiopathological situations. There are low concentrations of circulating thyroid hormone and very high concentrations of TRH and pTRH-(160–169) during development, and experimental hypothyroidism results in higher concentrations of prepro (pp)-TRH messenger RNA (mRNA) and TRH content in the adult rat pancreas than are present in the euthyroid pancreas.

The present study was carried out to investigate the interaction between T₃ and pancreatic TRH during the functional maturation of islets in culture and to validate the data obtained in vivo.

T₃ decreases ppTRH mRNA in islets in a dose-dependent manner. The primary impact of T₃ on islet function may be mediated by ppTRH mRNA, as short term T₃ treatment had no effect. Long term T₃ treatment reduced the islet TRH content and the amounts of pTRH-(160–169) and insulin released. This secretory pattern and coordinated regulation of pTRH-(160–169) and insulin suggests that pTRH-(160–169) plays a specific role in the regulation of insulin secretion.

This article has been cited by other articles:

				H. Oberkofler, K. Klein, T. K. Felder, F. Krempler, and W. Patsch Role of Peroxisome Proliferator-Activated Receptor-{gamma} Coactivator-1{alpha} in the Transcriptional Regulation of the Human Uncoupling Protein 2 Gene in INS-1E Cells Endocrinology, February 1, 2006; 147(2): 966 - 976. [Abstract] [Full Text] [PDF]

				G M Ledda-Columbano, A Perra, M Pibiri, F Molotzu, and A Columbano Induction of pancreatic acinar cell proliferation by thyroid hormone J. Endocrinol., June 1, 2005; 185(3): 393 - 399. [Abstract] [Full Text] [PDF]