Evidence map›Paper›PMID 34502119›Full record

ReviewInternational journal of molecular sciences2021

Multiple Leptin Signalling Pathways in the Control of Metabolism and Fertility: A Means to Different Ends?

Maggie C Evans, Rebecca A Lord, Greg M Anderson

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. The role of leptin in the male reproductive system.Journal of the Turkish German Gynecological Association · 2024
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Mitochondrial Unfolded Protein Response GeneInternational journal of molecular sciences · 2024
    Article
  18. Review
  19. Article
  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

3 authors at 1 institution in 1 country.

Maggie C EvansCentre for Neuroendocrinology, Department of Anatomy, University of Otago, Dunedin 9016, New Zealand.
Rebecca A LordCentre for Neuroendocrinology, Department of Anatomy, University of Otago, Dunedin 9016, New Zealand.
Greg M AndersonCentre for Neuroendocrinology, Department of Anatomy, University of Otago, Dunedin 9016, New Zealand.
University of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adipocyte-derived 'satiety promoting' hormone, leptin, has been identified as a key central regulator of body weight and fertility, such that its absence leads to obesity and infertility. Plasma leptin levels reflect body adiposity, and therefore act as an 'adipostat', whereby low leptin levels reflect a state of low body adiposity (under-nutrition/starvation) and elevated leptin levels reflect a state of high body adiposity (over-nutrition/obesity). While genetic leptin deficiency is rare, obesity-related leptin resistance is becoming increasingly common. In the absence of adequate leptin sensitivity, leptin is unable to exert its 'anti-obesity' effects, thereby exacerbating obesity. Furthermore, extreme leptin resistance and consequent low or absent leptin signalling resembles a state of starvation and can thus lead to infertility. However, leptin resistance occurs on a spectrum, and it is possible to be resistant to leptin's metabolic effects while retaining leptin's permissive effects on fertility. This may be because leptin exerts its modulatory effects on energy homeostasis and reproductive function through discrete intracellular signalling pathways, and these pathways are differentially affected by the molecules that promote leptin resistance. This review discusses the potential mechanisms that enable leptin to exert differential control over metabolic and reproductive function in the contexts of healthy leptin signalling and of diet-induced leptin resistance.

Indexed as

Energy MetabolismSignal TransductionBiomarkersDisease SusceptibilityFertilityGene Expression RegulationHumansLeptinPhosphatidylinositol 3-KinasesProtein BindingProto-Oncogene Proteins c-aktReceptors, LeptinSTAT3 Transcription FactorTOR Serine-Threonine KinasesBiomarkersLeptinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, LeptinSTAT3 Transcription FactorTOR Serine-Threonine KinasesAktCRTCfertilityleptinleptin resistancemetabolismPI3Ksignalling pathwaysSTAT3

Identifiers

PMID34502119
PMCPMC8430761
OpenAlexW3193447455

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.