Reference : Low TSH requirement and goiter in transgenic mice overexpressing IGF-1 and IGF-1R in ...
Scientific journals : Article
Life sciences : Genetics & genetic processes
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/4980
Low TSH requirement and goiter in transgenic mice overexpressing IGF-1 and IGF-1R in the thyroid gland
English
Clément, S. [Université Libre de Bruxelles - ULB > Institut de Recherche Interdisciplinaire en Biologie Humaine et Nucléaire, Institut de Biologie et de Médecine Moléculaire > > > >]
Refetoff, S. [Departments of Medicine and Pediatrics, University of Chicago (S.R.), Chicago, Illinois 60637 > > > >]
Robaye, B. [Université Libre de Bruxelles - ULB > Institut de Recherche Interdisciplinaire en Biologie Humaine et Nucléaire, Institut de Biologie et de Médecine Moléculaire > > > >]
Dumont, E. [Université Libre de Bruxelles - ULB > Institut de Recherche Interdisciplinaire en Biologie Humaine et Nucléaire, Institut de Biologie et de Médecine Moléculaire > > > >]
Schurmans, Stéphane mailto [Université Libre de Bruxelles - ULB > Institut de Recherche Interdisciplinaire en Biologie Humaine et Nucléaire, Institut de Biologie et de Médecine Moléculaire > > > >]
2001
Endocrinology
Endocrine Society
142
12
5131-5139
Yes (verified by ORBi)
International
0013-7227
1945-7170
Chevy Chase
MD
[en] Through the cAMP signaling pathway, TSH stimulates thyroid follicular cell proliferation, differentiation, and function. Although the autocrine production of IGF-I in the thyroid gland suggests an important physiological function for this factor in these processes, the exact role of the IGF-I/IGF-I receptor system in vivo remains unclear. Although the mitogenic action of TSH requires the presence of IGF-I or insulin in primary culture of dog and human thyroid cells, IGF-I has an effect equal to and independent of the effect of TSH on cell proliferation in rat thyroid cell lines and may even be the main growth regulator in this case. To investigate the in vivo function of the IGF-I/IGF-I receptor system, transgenic mice overexpressing human IGF-I, IGF-I receptor, or both in the thyroid were generated. Adult transgenic mice did not present external signs of thyroid dysfunction, but mice overexpressing both transgenes had significantly increased gland weight and follicular lumen area. A decreased TSH level together with a slightly increased serum T4 concentration and increased thyroidal iodine uptake were also observed, suggesting that IGF-I and IGF-I receptor stimulate thyroid function to some extent in vivo
Researchers ; Professionals
http://hdl.handle.net/2268/4980
10.1210/endo.142.12.8534

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