Evidence map›Paper›PMID 23685313›Full record

ReviewBiochimica et biophysica acta2014

Direct and indirect effects of leptin on adipocyte metabolism.

Ruth B S Harris

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 3 pooled it
5.5field-weighted citation impact, top 3% 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

128 citing papers in PubMed, 3 syntheses or guidelines pooled it, 302 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Article
  7. Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026
    Review
  8. Review
  9. Leveraging Multiomic Signatures to Predict Body Composition.Advances in nutrition (Bethesda, Md.) · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Integrative Adipogenic Engineering of Cultured Fat for Cell Based Meat.Comprehensive reviews in food science and food safety · 2026
    Review
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Heat-InactivatedInternational journal of molecular sciences · 2025
    Article
  20. Review

68 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

1 author at 1 institution in 1 country.

Ruth B S HarrisDepartment of Physiology, Medical College of Georgia, Georgia Regents University, USA. Electronic address: ruharris@GRU.edu.
Augusta University · US

Funding

LEPTIN AND PERIPHERAL GLUCOSE METABOLISMR01DK053903 · NIDDK · UNIVERSITY OF GEORGIA (UGA) · PI HARRIS, RUTH B · 1999 to 2018
$4.6M
NIDDK NIH HHS DK053903NIDDK NIH HHS R01 DK053903
6 · The paper itself

Abstract

Leptin is hypothesized to function as a negative feedback signal in the regulation of energy balance. It is produced primarily by adipose tissue and circulating concentrations correlate with the size of body fat stores. Administration of exogenous leptin to normal weight, leptin responsive animals inhibits food intake and reduces the size of body fat stores whereas mice that are deficient in either leptin or functional leptin receptors are hyperphagic and obese, consistent with a role for leptin in the control of body weight. This review discusses the effect of leptin on adipocyte metabolism. Because adipocytes express leptin receptors there is the potential for leptin to influence adipocyte metabolism directly. Adipocytes also are insulin responsive and receive sympathetic innervation, therefore leptin can also modify adipocyte metabolism indirectly. Studies published to date suggest that direct activation of adipocyte leptin receptors has little effect on cell metabolism in vivo, but that leptin modifies adipocyte sensitivity to insulin to inhibit lipid accumulation. In vivo administration of leptin leads to a suppression of lipogenesis, an increase in triglyceride hydrolysis and an increase in fatty acid and glucose oxidation. Activation of central leptin receptors also contributes to the development of a catabolic state in adipocytes, but this may vary between different fat depots. Leptin reduces the size of white fat depots by inhibiting cell proliferation both through induction of inhibitory circulating factors and by contributing to sympathetic tone which suppresses adipocyte proliferation. This article is part of a Special Issue entitled: Modulation of Adipose Tissue in Health and Disease.

Indexed as

AdipocytesAdipose TissueAnimalsBody Fat DistributionBody WeightEatingEnergy MetabolismHumansLeptinMiceLeptinInsulinLeptin receptorLipogenesisLipolysisSympathetic nervous system

Identifiers

PMID23685313
PMCPMC3838442
OpenAlexW2109449750

What Socratic 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 Socratic graph.