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Study · Not a test of the peptide alone · 1996

1 result

Thyrotropin via cyclic AMP induces insulin receptor expression and insulin Co-stimulation of growth and amplifies insulin and insulin-like growth factor signaling pathways in dog thyroid epithelial cells.

Burikhanov R, Coulonval K, Pirson I, Lamy F, Dumont JE, Roger PP

The Journal of biological chemistry1 Nov 1996Cited by 35 (Europe PMC)

PMID8910605 (opens in a new tab)DOI10.1074/jbc.271.46.29400 (opens in a new tab)PepBankPUB-08910605
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Summary

Despite the similarity of their receptors and signal transduction pathways, insulin is regarded as a regulator of glucose, protein, and lipid metabolism, whereas insulin-like growth factors (IGF-I and IGF-II) mainly act as mitogenic hormones. In the dog thyroid primary culture model, the triggering of DNA synthesis by thyrotropin (TSH) through cAMP, or by cAMP-independent factors including epidermal growth factor, hepatocyte growth factor and phorbol esters, requires insulin or IGFs as comitogenic factors. In the present study, in TSH-treated cells, IGF-I receptors and insulin receptors were paradoxically equivalent in their capacity to elicit the comitogenic pathway, which, however, was mediated only by IGF-I receptors in dog thyroid cells stimulated by cAMP-independent mitogens. Moreover, prior cell exposure to TSH or forskolin increased their responsiveness to insulin, IGF-I, and IGF-II, as seen on DNA synthesis and activation of a common insulin/IGF signaling pathway. To understand these observations, binding characteristics and expression of insulin and IGF-I receptors were examined. To analyze IGF-I receptor characteristics, the unexpected interference of a huge presence of IGF-binding proteins at the cell membrane was avoided using labeled Long R3 IGF-I instead of IGF-I. Strikingly, TSH, through cAMP, time-dependently induced insulin binding and insulin receptor mRNA and protein accumulation without any effect on IGF-I receptors. These findings constitute a first example of an induction of insulin receptor gene expression by a cAMP-mediated hormone. In dog thyroid cells, this allows low physiological insulin concentrations to act as a comitogenic factor and might explain in part the enhanced responsiveness to IGFs in response to TSH. This raises the possibility that TSH-insulin interactions may play a role in the regulation of thyroid growth and function in vivo.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone1

In this study, IGF-1 LR3 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking IGF-1 LR3.

  1. 01LabNot a test of IGF-1 LR3 aloneIn vitro (cells)Mechanism

    In dog thyroid cells, thyrotropin acting through cAMP did not change IGF-I receptors, which were measured with labeled Long R3 IGF-I.

    In plain wordsIn dog thyroid cells, thyrotropin did not change IGF-I receptors. Long R3 IGF-I was only the labeled tool used to measure them.

    Peptide
    IGF-1 LR3
    Outcome
    No significant changeIGF-I receptor binding after thyrotropin (measured with labeled Long R3 IGF-I)
    Study

    dogn: not reported in source

    Dog thyroid primary cell culture
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    Strikingly, TSH, through cAMP, time-dependently induced insulin binding and insulin receptor mRNA and protein accumulation without any effect on IGF-I receptors.
    2 context sentences
    Summary · context
    To analyze IGF-I receptor characteristics, the unexpected interference of a huge presence of IGF-binding proteins at the cell membrane was avoided using labeled Long R3 IGF-I instead of IGF-I.
    Summary · context
    In the dog thyroid primary culture model, the triggering of DNA synthesis by thyrotropin (TSH) through cAMP, or by cAMP-independent factors including epidermal growth factor, hepatocyte growth factor and phorbol esters, requires insulin or IGFs as comitogenic factors.

    In this study, IGF-1 LR3 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking IGF-1 LR3.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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