Evidence map›Paper›PMID 11960027›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Resting and circadian release of nitric oxide is controlled by leptin in male rats.

C A Mastronardi, W H Yu, S M McCann

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-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

22 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. IncreasedFrontiers in physiology · 2018
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. High fat feeding impairs endothelin-1 mediated vasoconstriction through increased iNOS-derived nitric oxide.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2011
    Article
  17. Review
  18. Article
  19. Review
  20. Pressed for time: the circadian clock and hypertension.Journal of applied physiology (Bethesda, Md. : 1985) · 2009
    Review
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

3 authors at 2 institutions in 1 country.

C A MastronardiPennington Biomedical Research Center, Louisiana State University, 6400 Perkins Road, Baton Rouge, LA 70808-4124, USA.
W H Yu
S M McCann
Louisiana State University · USPennington Biomedical Research Center · US

Funding

MECHANISM OF ACTION OF CYTOKINES ON BRAIN AND PITUITARYR37MH051853 · NIMH · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MCCANN, SAMUEL M · 1995 to 2002
$870k
NIMH NIH HHS MH51853
6 · The paper itself

Abstract

Because leptin stimulates nitric oxide (NO) release from the hypothalamus and anterior pituitary gland, we hypothesized that it also might release NO from adipocytes, the principal source of leptin. Consequently, plasma concentrations of leptin and NO, estimated from its metabolites NO(3) and NO(2) (NO(3)-NO(2)), were measured in adult male rats. There was a linear increase of both leptin and NO(3)-NO(2) with body weight that was associated with a parallel rise in fat mass. These findings indicate that release of leptin and NO is directly related to adipocyte mass. Furthermore, there was a parallelism in circadian rhythm of both substances, with peaks at 0130 h and nadirs at 0730 h. Measurement of both leptin and NO(3)-NO(2) in plasma from individual rats revealed that NO(3)-NO(2) increased linearly with leptin. Incubation of epididymal fat pads with leptin or its i.v. injection in conscious rats increased NO(3)-NO(2) release. The release of NO(3)-NO(2) in vivo and in vitro exceeded that of leptin by many fold, indicating that leptin activates NO synthase. Leptin increased tumor necrosis factor (TNF)-alpha release at a 100-fold lower dose than required for NO release in vitro and in vivo, suggesting that it also may participate in leptin-induced NO release. However, because many molecules of leptin were required to release a molecule of TNF-alpha in vivo and in vitro, we believe that leptin-induced TNF-alpha release is an associated phenomenon not involved in NO production. The results support the hypothesis that adipocytes play a major role in NO release by activating NO synthase in the adipocytes and the adjacent capillary endothelium.

Indexed as

Circadian RhythmAdipocytesAnimalsBody WeightDose-Response Relationship, DrugLeptinMaleModels, BiologicalNitric OxideRatsTime FactorsTumor Necrosis Factor-alphaLeptinNitric OxideTumor Necrosis Factor-alpha

Identifiers

PMID11960027
PMCPMC122838
OpenAlexW2042314507

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.