Evidence map›Paper›PMID 26484582›Full record

ReviewMolecular endocrinology (Baltimore, Md.)2016

Minireview: CNS Mechanisms of Leptin Action.

Jonathan N Flak, Martin G Myers

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular endocrinology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
6.9field-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

98 citing papers in PubMed, 170 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Gut-brain axis in health and brain disease.Chinese medical journal · 2026
    Review
  5. Advances in Adipose Tissue Biology.Endocrine reviews · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Sex-specific systemic metabolic predictors of resistance to calorie restriction-induced weight loss in obese diversity outbred mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

38 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.

Jonathan N FlakDivision of Metabolism, Endocrinology and Diabetes (J.N.F., M.G.M.), Department of Internal Medicine, and Department of Molecular and Integrative Physiology (M.G.M.), University of Michigan, Ann Arbor, Michigan 48109.
Martin G MyersDivision of Metabolism, Endocrinology and Diabetes (J.N.F., M.G.M.), Department of Internal Medicine, and Department of Molecular and Integrative Physiology (M.G.M.), University of Michigan, Ann Arbor, Michigan 48109.
University of Michigan–Ann Arbor · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OMARY, BISHR · 1986 to 2021
$22.5M
Training in Basic and Translational Digestive SciencesT32DK094775 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHN Y KAO, LINDA C. SAMUELSON · 2012 to 2026
$3.6M
Molecular Mechanisms of Leptin Receptor/Jak2 ActionR37DK056731 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 2008 to 2017
$3.5M
A Leptin-Regulated Brainstem Pathway That Controls Glucose and Energy HomeostasisR01DK098853 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 2014 to 2017
$1.4M
Brainstem LepRb neurons in the control of metabolismF32DK098833 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FLAK, JONATHAN NICHOLAS · 2013 to 2013
$49k
NIDDK NIH HHS DK098833NIDDK NIH HHS DK098853NIDDK NIH HHS F32 DK098833NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P30 DK034933NIDDK NIH HHS R01 DK098853NIDDK NIH HHS R37 DK056731NIDDK NIH HHS T32 DK094775
6 · The paper itself

Abstract

Leptin is an adipocytokine that circulates in proportion to body fat to signal the repletion of long-term energy stores. Leptin acts via its receptor, LepRb, on specialized neuronal populations in the brain (mainly in the hypothalamus and brainstem) to alter motivation and satiety, as well as to permit energy expenditure and appropriate glucose homeostasis. Decreased leptin, as with prolonged caloric restriction, promotes a powerful orexigenic signal, decreases energy use via a number of neuroendocrine and autonomic axes, and disrupts glucose homeostasis. Here, we review what is known about cellular leptin action and focus on the roles for specific populations of LepRb-expressing neurons for leptin action.

Indexed as

AnimalsBrainEnergy MetabolismHomeostasisHumansHypothalamusLeptinNeuronsReceptors, LeptinLeptinReceptors, Leptin

Identifiers

PMID26484582
PMCPMC4695630
OpenAlexW2205815423

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.