Evidence map›Paper›PMID 20881244›Full record

ArticleEndocrinology2010

Leptin induces phosphorylation of neuronal nitric oxide synthase in defined hypothalamic neurons.

Jose Donato, Renata Frazão, Makoto Fukuda, Claudia R Vianna, Carol F Elias

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

27 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  5. Article
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  7. Article
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  9. Review
  10. Review
  11. Article
  12. The role of leptin in health and disease.Temperature (Austin, Tex.) · 2017
    Review
  13. Article
  14. Review
  15. Review
  16. Role of the adipocyte-derived hormone leptin in reproductive control.Hormone molecular biology and clinical investigation · 2014
    Review
  17. Article
  18. Review
  19. A critical view of the use of genetic tools to unveil neural circuits: the case of leptin action in reproduction.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    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

5 authors at 1 institution in 1 country.

Jose DonatoDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Renata Frazão
Makoto Fukuda
Claudia R Vianna
Carol F Elias
The University of Texas Southwestern Medical Center · US

Funding

Mouse Phenotype Core, Project 9 of 10PL1DK081182 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI RUSSELL, DAVID W. · 2007 to 2011
$2.0M
Role of leptin-mediated PI3 Kinase signaling on reproductive controlR01HD061539 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI ELIAS, CAROL FUZETI · 2009 to 2013
$1.6M
NICHD NIH HHS HD061539NICHD NIH HHS R01 HD061539NIDDK NIH HHS PL1 DK081182
6 · The paper itself

Abstract

Studies have indicated that the neurotransmitter nitric oxide (NO) mediates leptin's effects in the neuroendocrine reproductive axis. However, the neurons involved in these effects and their regulation by leptin is still unknown. We aimed to determine whether NO neurons are direct targets of leptin and by which mechanisms leptin may influence neuronal NO synthase (nNOS) activity. Nicotinamide adenine dinucleotide phosphate diaphorase activity and leptin-induced phosphorylation of signal transducer and activator of transcription-3 immunoreactivity were coexpressed in subsets of neurons of the medial preoptic area, the paraventricular nucleus of the thalamus, the arcuate nucleus (Arc), the dorsomedial nucleus of the hypothalamus (DMH), the posterior hypothalamic area, the ventral premammillary nucleus (PMV), the parabrachial nucleus, and the dorsal motor nucleus of the vagus nerve. Fasting blunted nNOS mRNA expression in the medial preoptic area, Arc, DMH, PMV, and posterior hypothalamic area, and this effect was not restored by acute leptin administration. No difference in the number of neurons expressing nNOS immunoreactivity was noticed comparing hypothalamic sections of fed (wild type and ob/ob), fasted, and fasted leptin-treated mice. However, we found that in states of low leptin levels, as in fasting, or lack of leptin, as in ob/ob mice, the number of neurons expressing the phosphorylated form of nNOS is decreased in the Arc, DMH, and PMV. Notably, acute leptin administration to fasted wild-type mice restored the number of phosphorylated form of nNOS neurons to that observed in fed wild-type mice. Herein we identified the first-order neurons potentially involved in NO-mediated effects of leptin and demonstrate that leptin regulates nNOS activity predominantly through posttranslational mechanisms.

Indexed as

Analysis of VarianceAnimalsFastingFemaleHypothalamusImmunohistochemistryIn Situ HybridizationLeptinMiceNeuronsNitric Oxide Synthase Type IPhosphorylationLeptinNitric Oxide Synthase Type I

Identifiers

PMID20881244
PMCPMC2954713
OpenAlexW1994655923

What Socratic 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 Socratic graph.