ArticleAlcoholism, clinical and experimental research2013
Evidence for possible period 2 gene mediation of the effects of alcohol exposure during the postnatal period on genes associated with maintaining metabolic signaling in the mouse hypothalamus.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Altered circadian expression of clock genes and clock-regulatory epigenetic modifiers in saliva of children with fetal alcohol spectrum disorders.Scientific reports · 2024Article
- miRNA-383 and miRNA-384 Suppress Proopiomelanocortin Gene Expression in the Hypothalamus: Effects of Early Life Ethanol Exposure.Neuroendocrinology · 2023Article
- Review
- Clock genes × stress × reward interactions in alcohol and substance use disorders.Alcohol (Fayetteville, N.Y.) · 2015Review
- Alcohol disrupts sleep homeostasis.Alcohol (Fayetteville, N.Y.) · 2015Review
- Fetal alcohol exposure disrupts metabolic signaling in hypothalamic proopiomelanocortin neurons via a circadian mechanism in male mice.Endocrinology · 2014Article
- Circadian rhythms and addiction: mechanistic insights and future directions.Behavioral neuroscience · 2014Review
- Chronic alcohol consumption from adolescence-to-adulthood in mice--hypothalamic gene expression changes in the dilated cardiomyopathy signaling pathway.BMC neuroscience · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
backgroundAnimals exposed to alcohol during the developmental period develop circadian disturbances and metabolic problems that often persist during their adult period. In order to study whether alcohol and the circadian clock interact to alter metabolic signaling in the hypothalamus, we determined whether postnatal alcohol feeding in mice permanently alters metabolic sensing in the hypothalamus. Furthermore, we evaluated whether the effect of circadian disruption via Period 2 (Per2) gene mutation prevents alcohol's effects on metabolic signaling in the hypothalamus.
methodsPer2 mutant and wild-type male and female mice of the same genetic background were given a milk formula containing ethanol (EtOH; 11.34% vol/vol) from postnatal day (PD) 2 to 7 and used for gene expression and peptide level determinations in the hypothalamus at PD7 and PD90.
resultsWe report here that postnatal alcohol feeding reduces the expression of proopiomelanocortin (Pomc) gene and production of β-endorphin and α-melanocyte stimulating hormone (α-MSH) in the hypothalamus that persists into adulthood. In addition, expressions of metabolic sensing genes in the hypothalamus were also reduced as a consequence of postnatal alcohol exposure. These effects were not sex-specific and were observed in both males and females. Mice carrying a mutation of the Per2 gene did not show any reductions in hypothalamic levels of Pomc and metabolic genes and β-endorphin and α-MSH peptides following alcohol exposure.
conclusionsThese data suggest that early-life exposure to alcohol alters metabolic sensing to the hypothalamus possibly via regulating Per2 gene and/or the cellular circadian clock mechanism.
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