Prenatal ethanol exposure alters the expression of period genes governing the circadian function of β‐endorphin neurons in the hypothalamus

Chen, Cui Ping; Kühn, Peter; Advis, J. P.; Sarkar, Dipak K.

doi:10.1111/j.1471-4159.2006.03839.x

Cited by 45 publications

(62 citation statements)

References 34 publications

(31 reference statements)

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“…We observed an altered expression of the period genes Per1 and Per2 as well as a long-term altered cyclical expression of Pomc [61]. Altered sleep-wake cycles have previously been observed in human infants and adolescents exposed to alcohol during neurodevelopment [61]. Consistent with this study and others, these effects are most pronounced in animal models when exposure occurs during the brain growth spurt period [62,63].…”

Section: Discussionsupporting

confidence: 84%

“…Interestingly, this is associated with altered circadian rhythm signaling, as identified in both the short- and long-term canonical pathways. We observed an altered expression of the period genes Per1 and Per2 as well as a long-term altered cyclical expression of Pomc [61]. Altered sleep-wake cycles have previously been observed in human infants and adolescents exposed to alcohol during neurodevelopment [61].…”

Section: Discussionmentioning

confidence: 93%

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Third Trimester-Equivalent Ethanol Exposure Is Characterized by an Acute Cellular Stress Response and an Ontogenetic Disruption of Genes Critical for Synaptic Establishment and Function in Mice

Kleiber

Laufer²,

Stringer³

et al. 2014

Dev Neurosci

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The developing brain is remarkably sensitive to alcohol exposure, resulting in the wide range of cognitive and neurobehavioral characteristics categorized under the term fetal alcohol spectrum disorders (FASD). The brain is particularly susceptible to alcohol during synaptogenesis, a process that occurs heavily during the third trimester and is characterized by the establishment and pruning of neural circuitry; however, the molecular response of the brain to ethanol during synaptogenesis has not been documented. To model a binge-like exposure during the third-trimester neurodevelopmental equivalent, neonate mice were given a high (5 g/kg over 2 h) dose of ethanol at postnatal day 7. Acute transcript changes within the brain were assessed using expression arrays and analyzed for associations with gene ontology functional categories, canonical pathways, and gene network interactions. The short-term effect of ethanol was characterized by an acute stress response and a downregulation of energetically costly cellular processes. Further, alterations to a number of genes with roles in synaptic transmission and hormonal signaling, particularly those associated with the neuroendocrine development and function, were evident. Ethanol exposure during synaptogenesis was also associated with altered histone deacetylase and microRNA transcript levels, suggesting that abnormal epigenetic patterning may maintain some of the persistent molecular consequences of developmental ethanol exposure. The results shed insight into the sensitivity of the brain to ethanol during the third-trimester equivalent and outline how ethanol-induced alterations to genes associated with neural connectivity may contribute to FASD phenotypes.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 93%

Third Trimester-Equivalent Ethanol Exposure Is Characterized by an Acute Cellular Stress Response and an Ontogenetic Disruption of Genes Critical for Synaptic Establishment and Function in Mice

Kleiber

Laufer²,

Stringer³

et al. 2014

Dev Neurosci

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“…Increased miR-467b-5p in Slc17a6 promoter resulting in hypomethylation of hippocampal H3K4me3 at the Slc17a6 promoter, with corresponding increased mRNA levels of hippocampal Slc17a6, although its protein product VGLUT2 was decreased Rat Maternal ethanol exposure during pregnancy [110,112,114,128,[268][269][270][271] Behavioral, learning and memory deficits, and decreased birth and brain weights, and incisor emergence [284] Hypomethylation of the sperm LINE-1 gene Human/ cohort study Maternal exposure to organophosphate pesticides and persistent organic pollutants [291] Decreased adiponectin levels with increasing levels of cord blood p,p′-dichlorodiphenyl dichloroethene (DDE) in female offsprings…”

Section: Hypomethylation Of the Pancreatic Il13ra2 Genementioning

confidence: 99%

“…[264] Prenatal exposure to alcohol is demonstrated to induce extensive DNA methylation changes in human [265][266][267] and rodent offsprings ( Table 2). [110,112,114,120,128,[268][269][270][271][272] These effects are possibly transmitted via methylation of the paternal germ line, [273] although alcohol-induced placental epigenetic changes suggest the involvement of the female germ line. [264] The rising harmful use of alcohol, [274] just as tobacco use, [275] imposes a huge public health burden, and may have contributed in shaping the history of some NCCDs in recent years.…”

Section: Smoking Alcohol Pollutants and Other Environmental Chemicalsmentioning

confidence: 99%

The Impact of Traditional Food and Lifestyle Behavior on Epigenetic Burden of Chronic Disease

Imam

Ismail

2017

Global Challenges

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There are already extensive reviews on the global burden of NCCDs in the public domain. [1][2][3][4][5][6] The consensus that can be surmised from the available data on NCCDs is that their overall prevalence appears to be rising globally and the projections indicate an upward trend. Epidemiological transition data suggests that the morbidity and mortality rate from these diseases is far more than that of communicable diseases in the developed world [7] and a similar trend is now occurring in the low to medium income countries (LMICs). [8] Among the NCCDs, cardiovascular diseases (CVDs) are the leading causes of morbidity and mortality, followed closely by metabolic diseases like Noncommunicable chronic diseases (NCCDs) are the leading causes of morbidity and mortality globally. The mismatch between present day diets and ancestral genome is suggested to contribute to the NCCDs burden, which is promoted by traditional risk factors like unhealthy diets, physical inactivity, alcohol and tobacco. However, epigenetic evidence now suggests that cumulatively inherited epigenetic modifications may have made humans more prone to the effects of present day lifestyle factors. Perinatal starvation was widespread in the 19th century. This together with more recent events like increasing consumption of western and low fiber diets, smoking, harmful use of alcohol, physical inactivity, and environmental pollutants may have programed the human epigenome for higher NCCDs risk. In this review, on the basis of available epigenetic data it is hypothesized that transgenerational effects of lifestyle factors may be contributing to the current global burden of NCCDs. Thus, there is a need to reconsider prevention strategies so that the subsequent generations will not have to pay for our sins and those of our ancestors. Cardiovascular DiseasesDr. M. U. Imam

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“…Diferentes sustancias parecen responder de forma diferente en aquellos sujetos con historia familiar de alcoholismo: adrenocorticotropic hormone (ACTH), cortisol (CORT) y prolactina (PRL) (14,15),[aunque estudios posteriores desmienten el comportamiento previo señalado para CORT (13) y para PRL (12)], así como el alcohol puede alterar el ritmo circadiano y sus controles (38,39).…”

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Niveles de beta-endorfinas en hijos de padres alcohólicos

Arbol¹,

Irles²,

Contreras³

et al. 2007

An. Med. Interna (Madrid)

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RESUMENIntroducción: En los últimos años son numerosos los trabajos acerca de las posibles causas del alcoholismo, donde parece intervenir varios factores, siendo la herencia uno de los más implicados, aunque se han destacado otros, como factores ambientales, que contribuirían a aumentar o disminuir el riesgo individual para desarrollar una dependencia alcohó-lica.Método: Para intentar aclarar la posible influencia de la herencia en el alcoholismo, hemos estudiado los niveles de beta-endorfinas (β-E) en 25 familias de alcohólicos, en las cuales había 27 hijos con un padre alcohólico y 7 hijos con los dos, así como en dichos padres alcohólicos, y comparado los resultados con unos grupos control: uno de adultos no bebedores y otro de niños normales en familias de no-bebedores, con edades similares.Resultados: Se ha encontrado que los hijos de alcohólicos tienen unos niveles de β-E significativamente más bajos (p < 0,001) que los controles, y estos niveles eran aún más bajos en los hijos cuyos dos padres eran alcohólicos.Conclusión: Se concluye que la determinación de β-E podía tener un valor predictivo a la hora de determinar quién es más propenso a ser alcohólico en el futuro.

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Prenatal ethanol exposure alters the expression of period genes governing the circadian function of β‐endorphin neurons in the hypothalamus

Cited by 45 publications

References 34 publications

Third Trimester-Equivalent Ethanol Exposure Is Characterized by an Acute Cellular Stress Response and an Ontogenetic Disruption of Genes Critical for Synaptic Establishment and Function in Mice

Third Trimester-Equivalent Ethanol Exposure Is Characterized by an Acute Cellular Stress Response and an Ontogenetic Disruption of Genes Critical for Synaptic Establishment and Function in Mice

The Impact of Traditional Food and Lifestyle Behavior on Epigenetic Burden of Chronic Disease

Niveles de beta-endorfinas en hijos de padres alcohólicos

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