Evidence map›Paper›PMID 19022883›Full record

ArticleEndocrinology2009

Reversal of physiological deficits caused by diminished levels of peptidylglycine alpha-amidating monooxygenase by dietary copper.

D Bousquet-Moore, X M Ma, E A Nillni, T A Czyzyk, J E Pintar, B A Eipper, R E Mains

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  4. Germline loss-of-functionmedRxiv : the preprint server for health sciences · 2023
    Article
  5. Germline loss-of-functionFrontiers in endocrinology · 2023
    Article
  6. Peptidylglycine α-amidating monooxygenase is required for atrial secretory granule formation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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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

7 authors at 3 institutions in 1 country.

D Bousquet-MooreDepartment of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut 06030-3401, USA.
X M Ma
E A Nillni
T A Czyzyk
J E Pintar
B A Eipper
R E Mains
UConn Health · USJohnson University · USRhode Island Hospital · US

Funding

BIOCHEMISTRY AND PHYSIOLOGY OF PEPTIDE AMIDATIONR01DK032949 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH ANNE, KING, STEPHEN M · 1986 to 2017
$6.4M
BIOCHEMISTRY AND PHYSIOLOGY OF PEPTIDE AMIDATIONR37DK032949 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH A · 1989 to 2004
$2.8M
BIOCHEMISTRY AND PHYSIOLOGY OF PEPTIDE AMIDATIONR56DK032949 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH A · 2005 to 2005
$104k
Genetic Reduction in Peptide Amidation Results in Neuroendocrine DeficitsF31MH080589 · NIMH · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MOORE, DANIELLE BOUSQUET · 2007 to 2009
$56k
NIDDK NIH HHS DK32949NIDDK NIH HHS R01 DK032949NIDDK NIH HHS R37 DK032949NIDDK NIH HHS R56 DK032949NIMH NIH HHS F31 MH080589NIMH NIH HHS MH080589
6 · The paper itself

Abstract

Amidated peptides are critically involved in many physiological functions. Genetic deletion of peptidylglycine alpha-amidating monooxygenase (PAM), the only enzyme that can synthesize these peptides, is embryonically lethal. The goal of the present study was the identification of physiological functions impaired by haploinsufficiency of PAM. Regulation of the hypothalamic-pituitary-thyroid axis and body temperature, functions requiring contributions from multiple amidated peptides, were selected for evaluation. Based on serum T(4) and pituitary TSH-beta mRNA levels, mice heterozygous for PAM (PAM(+/-)) were euthyroid at baseline. Feedback within the hypothalamic-pituitary-thyroid axis was impaired in PAM(+/-) mice made hypothyroid using a low iodine/propylthiouracil diet. Despite their normal endocrine response to cold, PAM(+/-) mice were unable to maintain body temperature as well as wild-type littermates when kept in a 4 C environment. When provided with additional dietary copper, PAM(+/-) mice maintained body temperature as well as wild-type mice. Pharmacological activation of vasoconstriction or shivering also allowed PAM(+/-) mice to maintain body temperature. Cold-induced vasoconstriction was deficient in PAM(+/-) mice. This deficit was eliminated in PAM(+/-) mice receiving a diet with supplemental copper. These results suggest that dietary deficiency of copper, coupled with genetic deficits in PAM, could result in physiological deficits in humans.

Indexed as

Adipose Tissue, BrownAnimalsBody TemperatureCold TemperatureCopperDietary SupplementsFemaleGenotypeHypothalamusIon ChannelsMaleMiceMice, Mutant StrainsMitochondrial ProteinsMixed Function OxygenasesMultienzyme ComplexesCopperIon ChannelsMitochondrial ProteinsMixed Function OxygenasesMultienzyme ComplexesN-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamidepeptidylglycine monooxygenasePhenylephrinePiperazinesPyridinesUncoupling Protein 1

Identifiers

PMID19022883
PMCPMC2659272
OpenAlexW2001473326

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.