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

Title:
Fetal alcohol programming of hypothalamic proopiomelanocortin system by epigenetic mechanisms and later life vulnerability to stress.
Authors:
Bekdash R; Endocrinology 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., Zhang C, Sarkar D
Source:
Alcoholism, clinical and experimental research [Alcohol Clin Exp Res] 2014 Sep; Vol. 38 (9), pp. 2323-30. Date of Electronic Publication: 2014 Jul 28.
Publication Type:
Journal Article; Research Support, N.I.H., Extramural; Review
Language:
English
Journal Info:
Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 7707242 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1530-0277 (Electronic) Linking ISSN: 01456008 NLM ISO Abbreviation: Alcohol Clin Exp Res Subsets: MEDLINE
Imprint Name(s):
Publication: Oxford, UK : Wiley-Blackwell
Original Publication: New York, N.Y. : Grune & Stratton, c1977-
MeSH Terms:
Epigenesis, Genetic/*physiology , Fetal Alcohol Spectrum Disorders/*genetics , Fetal Development/*physiology , Hypothalamo-Hypophyseal System/*physiology , Pro-Opiomelanocortin/*genetics , Stress, Psychological/*genetics, Adult ; Animals ; Female ; Fetal Alcohol Spectrum Disorders/epidemiology ; Fetal Alcohol Spectrum Disorders/metabolism ; Humans ; Nerve Net/physiology ; Pituitary-Adrenal System/physiology ; Pregnancy ; Prenatal Exposure Delayed Effects/epidemiology ; Prenatal Exposure Delayed Effects/genetics ; Prenatal Exposure Delayed Effects/metabolism ; Pro-Opiomelanocortin/metabolism ; Stress, Psychological/epidemiology ; Stress, Psychological/metabolism
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Grant Information:
R21 AA016695 United States AA NIAAA NIH HHS; R37 AA008757 United States AA NIAAA NIH HHS; R37AA08757 United States AA NIAAA NIH HHS; R01AA016695 United States AA NIAAA NIH HHS
Contributed Indexing:
Keywords: Epigenetics; Fetal Alcohol; Proopiomelanocortin; Stress; Transgenerational
Substance Nomenclature:
66796-54-1 (Pro-Opiomelanocortin)
Entry Date(s):
Date Created: 20140730 Date Completed: 20150622 Latest Revision: 20211021
Update Code:
20250114
PubMed Central ID:
PMC4177357
DOI:
10.1111/acer.12497
PMID:
25069392
Database:
MEDLINE

Weitere Informationen

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.
(Copyright © 2014 by the Research Society on Alcoholism.)