Cited by 74Thyroid Disorders and TreatmentsNeuropeptides and Animal PhysiologyHypothalamic control of reproductive hormones

Suppression of Thyrotropin-Releasing Hormone Gene Expression by lnterleukin-1-Beta in the Rat: Implications for Nonthyroidal Illness

Kakucska, Ildikó, Romero, Luz I., Clark, Burton D., Rondeel, Jan M.M., Qi, Yanping, Alex, Sharon, Emerson, Charles H., Lechan, Ronald M.·2008·Neuroendocrinology

Abstract

Nonthyroidal illness is characterized by low thyroid hormone levels and inappropriately normal or decreased TSH levels. To determine whether the hypothalamus contributes to these responses, TRH gene expression in hypophysiotropic neurons of the paraventricular nucleus (PVN) was investigated using semiquantitative in situ hybridization histochemistry in an animal model of nonthyroidal illness. Following the systemic administration of bacterial lipopolysaccharide (LPS; 250 µg/100 g BW), plasma T 4, T 3 and TSH were reduced but this was not associated with an increase in the content of proTRH mRNA in the PVN as occurs when plasma T 4 and T 3 concentrations fall during primary hypothyroidism. Constant infusion of human interleukin-1β (IL-1β) into the cerebrospinal fluid also reduced plasma T 4 concentration. This persisted for the duration of the infusion but TSH was only suppressed after 7 days of infusion when body weight had declined. By 24 h, the content of proTRH mRNA in the PVN in IL-1β infused animals was significantly reduced from control values. These studies indicate that the peripheral administration of endotoxin or central administration of IL-1β in the rat is associated with a proTRH mRNA content in the PVN that may be inappropriately normal or reduced for the level of circulating thyroid hormone. We propose that the inability of hypophysiotropic neurons to induce TRH gene expression in nonthyroidal illness, when circulating thyroid hormone levels are low, is one of several factors that contributes to the inability of the anterior pituitary to increase its secretion of TSH.

Integrity signals

Registry

Crossref · 10.1159/000126649

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Reduced hypothalamic TRH expression, portal serum TRH and pituitary TSH content have been observed both in NTIS patients and NTIS animal models.

    “Indeed, reduced hypothalamic TRH expression, portal serum TRH and pituitary TSH content have been observed both in NTIS patients [65] and NTIS animal models [12, 19, 66, 67].”

    From An update on non-thyroidal illness syndrome (2021) · cites this paper as [67]

Cited by

Sorted by citations

Authors
Kakucska, I., Romero, L. I., Clark, B. D., Rondeel, J. M. M., Qi, Y., Alex, S., Emerson, C. H., & Lechan, R. M.
Affiliations
  • Tufts Medical Center (US)
  • University of Massachusetts Chan Medical School (US)
Venue
Neuroendocrinology
Publisher
S. Karger AG
Published
2008-04-08
Volume
59
Issue
2
Pages
129-137
ISSN
  • 0028-3835 (ISSN-L)
  • 1423-0194
OpenAlex
W1979796052
Cited by
74
References
0
Citations by year
2025: 1 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 1 · 2016: 4 · 2015: 2 · 2014: 1 · 2013: 3 · 2012: 1
FWCI
3.13
Type
journal article
Language
en
Open access
closed
Locations
  • Neuroendocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01dk027850-09)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 37021, DK-27850)
  • Division of Chemistry
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Keywords
low T3 syndrome, thyrotropin-releasing hormone, IL-1β, paraventricular nucleus, TSH secretion, lipopolysaccharide, endotoxin, thyroid hormones, anterior pituitary, hypothalamus, cerebrospinal fluid infusion
MeSH terms
Animals, Corticotropin-Releasing Hormone, Disease Models, Animal, Interleukin-1, Lipopolysaccharides, Male, Paraventricular Hypothalamic Nucleus, RNA, Messenger, Thyrotropin, Thyrotropin-Releasing Hormone, Thyroxine, Triiodothyronine, Gene Expression, Rats, Sprague-Dawley, In Situ Hybridization, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review