Evidence map›Paper›PMID 24862904›Full record

ReviewJournal of chemical neuroanatomy2014

The impact of leptin on perinatal development and psychopathology.

Jeanette C Valleau, Elinor L Sullivan

Open access · greenAbstract readReview
In one paragraph

Review in Journal of chemical neuroanatomy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 4 pooled it
1.9field-weighted citation impact, top 15% 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

52 citing papers in PubMed, 4 syntheses or guidelines pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  8. Molecular pathways in placental-fetal development and disruption.Molecular and cellular endocrinology · 2024
    Review
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  10. Observational
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  15. Microbiota-Gut-Brain Axis in Major Depression: A New Therapeutic Approach.Advances in experimental medicine and biology · 2023
    Review
  16. Article
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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.

Jeanette C ValleauDivision of Diabetes, Obesity and Metabolism, Oregon National Primate Research Center, 505 NW 185th Ave., Beaverton, OR, USA.
Elinor L SullivanDivision of Diabetes, Obesity and Metabolism, Oregon National Primate Research Center, 505 NW 185th Ave., Beaverton, OR, USA; Department of Biology, University of Portland, 5000 N Willamette Blvd., Portland, OR, USA. Electronic address: sullivae@up.edu.
Oregon National Primate Research Center · US

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI FRUH, KLAUS J · 1985 to 2011
$140.8M
Oregon Clinical and Translational Research InstituteUL1TR000128 · NCATS · OREGON HEALTH & SCIENCE UNIVERSITY · PI ELLISON, DAVID H · 2012 to 2015
$28.7M
Maternal High Fat Diet and Melanocortin System in OffspringR01DK079194 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI KIEVIT, PAUL · 2007 to 2015
$6.2M
NCATS NIH HHS UL1 TR000128NCATS NIH HHS UL1TR000128NCRR NIH HHS P51 RR000163NICHD NIH HHS L40 HD059242NIDDK NIH HHS R01 DK079194NIDDK NIH HHS R01DK079194
6 · The paper itself

Abstract

Leptin has long been associated with metabolism as it is a critical regulator of both food intake and energy expenditure, but recently, leptin dysregulation has been proposed as a mechanism of psychopathology. This review discusses the evidence supporting a role for leptin in mental health disorders and describes potential mechanisms that may underlie this association. Leptin plays a critical role in pregnancy and in fetal growth and development. Leptin's role and profile during development is examined in available human studies, and the validity of applying studies conducted in animal models to the human population are discussed. Rodents experience a postnatal leptin surge, which does not occur in humans or larger animal models. This suggests that further research using large mammal models, which have a leptin profile across pregnancy and development similar to humans, are of high importance. Maternal obesity and hyperleptinemia correlate with increased leptin levels in the umbilical cord, placenta, and fetus. Leptin levels are thought to impact fetal brain development; likely by activating proinflammatory cytokines that are known to impact many of the neurotransmitter systems that regulate behavior. Leptin is likely involved in behavioral regulation as leptin receptors are widely distributed in the brain, and leptin influences cortisol release, the mesoaccumbens dopamine pathway, serotonin synthesis, and hippocampal synaptic plasticity. In humans, both high and low levels of leptin are reported to be associated with psychopathology. This inconsistency is likely due to differences in the metabolic state of the study populations. Leptin resistance, which occurs in the obese state, may explain how both high and low levels of leptin are associated with psychopathology, as well as the comorbidity of obesity with numerous mental illnesses. Leptin resistance is likely to influence disorders such as depression and anxiety where high leptin levels have been correlated with symptomatology. Schizophrenia is also associated with both low and high leptin levels. However, as anti-psychotics pharmacotherapy induces weight gain, which elevates leptin levels, drug-naïve populations are needed for further studies. Elevated circulating leptin is consistently found in childhood neurodevelopmental disorders including autism spectrum disorders and Rhett disorder. Further, studies on the impact of leptin and leptin resistance on psychopathology and neurodevelopmental disorders are important directions for future research. Studies examining the mechanisms by which exposure to maternal obesity and hyperleptinemia during fetal development impact brain development and behavior are critical for the health of future generations.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsBrainFemaleHumansLeptinMental DisordersObesityPregnancyLeptinBehavioral regulationInflammationMental health disordersNeurodevelopmentObesityPregnancy

Identifiers

PMID24862904
PMCPMC4241386
OpenAlexW2059925368

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.