Evidence map›Paper›PMID 22225569›Full record

ArticleBritish journal of pharmacology2012

3-Iodothyronamine: a modulator of the hypothalamus-pancreas-thyroid axes in mice.

Maria Elena Manni, Gaetano De Siena, Alessandro Saba, Maja Marchini, Ilaria Dicembrini, Elisabetta Bigagli, Lorenzo Cinci, Maura Lodovici, Grazia Chiellini, Riccardo Zucchi and 1 more

Abstract read
In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. 3-Iodothyronamine and Derivatives: New Allies Against Metabolic Syndrome?International journal of molecular sciences · 2020
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Maria Elena ManniDepartment of Pharmacology, University of Florence, Florence, Italy Department of Biochemistry, University of Pisa, Pisa, Tuscany, Italy.
Gaetano De Siena
Alessandro Saba
Maja Marchini
Ilaria Dicembrini
Elisabetta Bigagli
Lorenzo Cinci
Maura Lodovici
Grazia Chiellini
Riccardo Zucchi
Laura Raimondi
University of Florence · ITUniversity of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND PURPOSE Preclinical pharmacology of 3-iodothyronamine (T1AM), an endogenous derivative of thyroid hormones, indicates that it is a rapid modulator of rodent metabolism and behaviour. Since T1AM undergoes rapid enzymatic degradation, particularly by MAO, we hypothesized that the effects of T1AM might be altered by inhibition of MAO. EXPERIMENTAL APPROACH We investigated the effects of injecting T1AM (i.c.v.) on (i) feeding behaviour, hyperglycaemia and plasma levels of thyroid hormones and (ii) T1AM systemic bioavailability, in overnight fasted mice, under control conditions and after pretreatment with the MAO inhibitor clorgyline. T1AM (1.3, 6.6, 13, 20 and 26 µg·kg(-1) ) or vehicle were injected i.c.v. in fasted male mice not pretreated or pretreated i.p. with clorgyline (2.5 mg·kg(-1) ). Glycaemia was measured by a glucorefractometer, plasma triiodothyronine (fT3) by a chemiluminescent immunometric assay, c-fos activation immunohistochemically and plasma T1AM by HPLC coupled to tandem-MS. KEY RESULTS T1AM, 1.3 µg·kg(-1) , produced a hypophagic effect (-24% vs. control) and reduced c-fos activation. This dose showed systemic bioavailability (0.12% of injected dose), raised plasma glucose levels and reduced peripheral insulin sensitivity (-33% vs. control) and plasma fT3 levels. These effects were not linearly related to the dose injected. Clorgyline pretreatment strongly increased the systemic bioavailability of T1AM and prevented the hyperglycaemia and reduction in fT3 induced by T1AM. CONCLUSIONS AND IMPLICATIONS T1AM induces central and peripheral effects including hyperglycaemia and a reduction in plasma fT3 levels in fasted mice. These effects critically depend on the concentration of T1AM or its metabolites in target organs.

Indexed as

AnimalsBlood GlucoseClorgylineEatingExenatideFastingHyperglycemiaHypoglycemic AgentsHypothalamusInsulin ResistanceMaleMiceMonoamine Oxidase InhibitorsPancreasPeptidesProto-Oncogene Proteins c-fos3-iodothyronamineBlood GlucoseClorgylineExenatideHypoglycemic AgentsMonoamine Oxidase InhibitorsPeptidesProto-Oncogene Proteins c-fosThyroid HormonesThyroninesVenoms

Identifiers

PMID22225569
PMCPMC3417495
OpenAlexW1739247397

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.