Evidence map›Paper›PMID 24878261›Full record

ReviewFree radical biology & medicine2014

Regulation of obesity and insulin resistance by nitric oxide.

Brian E Sansbury, Bradford G Hill

Open access · hybridAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 2% 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

126 citing papers in PubMed, 1 synthesis or guideline pooled it, 267 citations in OpenAlex.

  1. Pooled it
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  11. The role of gasotransmitters in Parkinson's disease: Interplay of nitric oxide, carbon monoxide, and hydrogen sulfide.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  12. Thermogenic Adipose ADH5 Counteracts Age-related Metabolic Decline.bioRxiv : the preprint server for biology · 2025
    Article
  13. Article
  14. Review
  15. Article
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  17. Article
  18. Review
  19. Targeting L-arginine/NO/cGMP/KFrontiers in pharmacology · 2025
    Review
  20. Review

66 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Brian E SansburyDiabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY 40202, USA; Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Bradford G HillDiabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY 40202, USA; Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY 40202, USA; Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40202, USA. Electronic address: bradford.hill@louisville.edu.
University of Louisville · US

Funding

Tumor Necrosis Factor Modulation of CPCsP01HL078825 · NHLBI · UNIVERSITY OF LOUISVILLE · PI BOLLI, ROBERTO · 2005 to 2021
$37.6M
Project 5 - Metabolomic Analysis of AtherothrombosisP20GM103492 · NIGMS · UNIVERSITY OF LOUISVILLE · PI HONG, KYUNG UK · 2012 to 2017
$13.8M
NHLBI NIH HHS HL078825NHLBI NIH HHS P01 HL078825NIGMS NIH HHS GM103492NIGMS NIH HHS P20 GM103492
6 · The paper itself

Abstract

Obesity is a risk factor for developing type 2 diabetes and cardiovascular disease and has quickly become a worldwide pandemic with few tangible and safe treatment options. Although it is generally accepted that the primary cause of obesity is energy imbalance, i.e., the calories consumed are greater than are utilized, understanding how caloric balance is regulated has proven a challenge. Many "distal" causes of obesity, such as the structural environment, occupation, and social influences, are exceedingly difficult to change or manipulate. Hence, molecular processes and pathways more proximal to the origins of obesity-those that directly regulate energy metabolism or caloric intake-seem to be more feasible targets for therapy. In particular, nitric oxide (NO) is emerging as a central regulator of energy metabolism and body composition. NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin-resistant patients, and increasing NO output has remarkable effects on obesity and insulin resistance. This review discusses the role of NO in regulating adiposity and insulin sensitivity and places its modes of action into context with the known causes and consequences of metabolic disease.

Indexed as

AdiposityBody CompositionDietEnergy IntakeEnergy MetabolismHumansHungerInsulin ResistanceNitric OxideNitric Oxide Synthase Type IIIObesitySatiety ResponseNitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanDiabeteseNOSFree radicalsInsulin resistanceMitochondriaNitric oxideObesity

Identifiers

PMID24878261
PMCPMC4112002
OpenAlexW2004580431

What OpenQuestion holds

Textmetadata
LicenceTDM
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.