Evidence map›Paper›PMID 25069392›Full record

ReviewAlcoholism, clinical and experimental research2014

Fetal alcohol programming of hypothalamic proopiomelanocortin system by epigenetic mechanisms and later life vulnerability to stress.

Rola Bekdash, Changqing Zhang, Dipak Sarkar

Open access · greenAbstract readReview
In one paragraph

Review in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Modeling the enigma of complex disease etiology.Journal of translational medicine · 2023
    Article
  6. Article
  7. Review
  8. Long-term spatial tracking of cells affected by environmental insults.Journal of neurodevelopmental disorders · 2020
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Emerging Role of Epigenetic Mechanisms in Alcohol Addiction.Alcoholism, clinical and experimental research · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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.

Rola BekdashEndocrinology Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Neuroscience Graduate Program, The State University of New Jersey, New Brunswick, New Jersey.
Changqing Zhang
Dipak Sarkar
Rutgers, The State University of New Jersey · US

Funding

Role of Opiates in Alcohol-Induced Neurotoxicity- Diversity supplementR37AA008757 · NIAAA · RUTGERS, THE STATE UNIV OF N.J. · PI SARKAR, DIPAK KUMAR · 2009 to 2018
$4.0M
Epigenetics of alcohol effects on stress axis developmentR21AA016695 · NIAAA · RUTGERS, THE STATE UNIV OF N.J. · PI SARKAR, DIPAK KUMAR · 2008 to 2009
$405k
NIAAA NIH HHS R01AA016695NIAAA NIH HHS R21 AA016695NIAAA NIH HHS R37 AA008757NIAAA NIH HHS R37AA08757
6 · The paper itself

Abstract

Hypothalamic proopiomelanocortin (POMC) neurons, one of the major regulators of the hypothalamic-pituitary-adrenal (HPA) axis, immune functions, and energy homeostasis, are vulnerable to the adverse effects of fetal alcohol exposure (FAE). These effects are manifested in POMC neurons by a decrease in Pomc gene expression, a decrement in the levels of its derived peptide β-endorphin and a dysregulation of the stress response in the adult offspring. The HPA axis is a major neuroendocrine system with pivotal physiological functions and mode of regulation. This system has been shown to be perturbed by prenatal alcohol exposure. It has been demonstrated that the perturbation of the HPA axis by FAE is long-lasting and is linked to molecular, neurophysiological, and behavioral changes in exposed individuals. Recently, we showed that the dysregulation of the POMC system function by FAE is induced by epigenetic mechanisms such as hypermethylation of Pomc gene promoter and an alteration in histone marks in POMC neurons. This developmental programming of the POMC system by FAE altered the transcriptome in POMC neurons and induced a hyperresponse to stress in adulthood. These long-lasting epigenetic changes influenced subsequent generations via the male germline. We also demonstrated that the epigenetic programming of the POMC system by FAE was reversed in adulthood with the application of the inhibitors of DNA methylation or histone modifications. Thus, prenatal environmental influences, such as alcohol exposure, could epigenetically modulate POMC neuronal circuits and function to shape adult behavioral patterns. Identifying specific epigenetic factors in hypothalamic POMC neurons that are modulated by fetal alcohol and target Pomc gene could be potentially useful for the development of new therapeutic approaches to treat stress-related diseases in patients with fetal alcohol spectrum disorders.

Indexed as

AdultAnimalsEpigenesis, GeneticFemaleFetal Alcohol Spectrum DisordersFetal DevelopmentHumansHypothalamo-Hypophyseal SystemNerve NetPituitary-Adrenal SystemPregnancyPrenatal Exposure Delayed EffectsPro-OpiomelanocortinStress, PsychologicalPro-OpiomelanocortinEpigeneticsFetal AlcoholProopiomelanocortinStressTransgenerational

Identifiers

PMID25069392
PMCPMC4177357
OpenAlexW2049687736

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.