Evidence map›Paper›PMID 17584844›Full record

ReviewThe Journal of physiology2007

Hypothalamic leptin regulation of energy homeostasis and glucose metabolism.

Gregory J Morton

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 110 citations in OpenAlex.

  1. Trial
  2. Trial
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  7. Review
  8. Adipose tissue metabolic changes in chronic kidney disease.Immunometabolism (Cobham, Surrey) · 2023
    Review
  9. Article
  10. Leptin signaling and leptin resistance.Medical review (2021) · 2022
    Review
  11. Hypothalamic control of energy expenditure and thermogenesis.Experimental & molecular medicine · 2022
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Gregory J MortonDepartment of Medicine, Harbourview Medical Center, University of Washington, Seattle, WA 98104, USA. gjmorton@u.washington.edu
University of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence suggests that food intake, energy expenditure and endogenous glucose production are regulated by hypothalamic areas that respond to a variety of peripheral signals. Therefore, in response to a reduction in energy stores or circulating nutrients, the brain initiates responses in order to promote positive energy balance to restore and maintain energy and glucose homeostasis. In contrast, in times of nutrient abundance and excess energy storage, key hypothalamic areas activate responses to promote negative energy balance (i.e. reduced food intake and increased energy expenditure) and decreased nutrient availability (reduced endogenous glucose production). Accordingly, impaired responses or 'resistance' to afferent input from these hormonal or nutrient-related signals would be predicted to favour weight gain and insulin resistance and may contribute to the development of obesity and type 2 diabetes.

Indexed as

Energy MetabolismSignal TransductionAnimalsDiabetes Mellitus, Type 2EatingFeedback, PhysiologicalGlucoseHomeostasisHumansHypothalamusInsulin ResistanceLeptinLiverObesityWeight GainGlucoseLeptin

Identifiers

PMID17584844
PMCPMC2277030
OpenAlexW2105604156

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.