Evidence map›Paper›PMID 41057899›Full record

ArticleBMC medical genomics2025

Alcohol exposure significantly influences gene expression in the hypothalamus, highlighting complex links with gonadotropin-releasing hormone signaling and thyroid hormone production in adolescent mice.

Guangtao Sun, Yujing Peng, Chenxu Hu, Yifan Zheng, Yu Cheng, Xunzhong Qi, Yuling Jin

Abstract read
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Article in BMC medical genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Guangtao Sun *Department of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, People's Republic of China.
Yujing Peng *Department of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, People's Republic of China.
Chenxu Hu *Department of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, People's Republic of China.
Yifan Zheng *Department of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, People's Republic of China.
Yu ChengDepartment of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, People's Republic of China.
Xunzhong QiDepartment of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, People's Republic of China. 617han@163.com.
Yuling JinDepartment of Neurology, The First Affiliated Hospital of Jiamusi University, Jiamusi, People's Republic of China. jinyuling_jms@163.com.

Funding

Talent Training Project for Basic Scientific Research of Heilongjiang Province Educational Commission of China 2021-KYYWF-0603
6 · The paper itself

Abstract

objectiveHypothalamic dysfunction occurs in alcohol use disorder (AUD). Here, we investigated the effects of alcohol exposure on hypothalamic gene expression in mice, and examined the role of the hypothalamus in AUD pathogenesis.

methodsAn alcohol exposure model was constructed in male C57BL/6 mice using the two-bottle drinking method. Transcriptome sequencing was used to analyze differential gene expression in the hypothalamus of alcohol exposure model and control mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of the differentially expressed genes were performed. In addition, real-time quantitative PCR was used to verify the differential expression of genes.

resultsWe identified 225 differentially expressed genes by transcriptome sequencing, of which 64 showed increased expression and 161 decreased expression. GO enrichment analysis showed highest enrichment for developmental process terms. KEGG enrichment analysis showed highest enrichment for the gonadotropin-releasing hormone (GnRH) signaling pathway. PCR validation showed reduced expression of Prkcd, Ptk2b, and Adcy1 in the alcohol group compared with the control group, consistent with the sequencing results. The thyroid hormone synthesis pathway was significantly enriched, and PCR results showed that expression of Adcy1, Gpx2, and Ttr were decreased in the alcohol group compared with the control group, which was consistent with the sequencing results.

conclusionAlcohol exposure in mice modulates the expression of genes associated with hypothalamic GnRH signaling pathway and thyroid hormone synthesis pathway. Expression of GnRH signaling pathway genes, Prkcd and Ptk2b, and of thyroid hormone synthesis pathway genes, Gpx2, Ttr, and Adcy1, was decreased. Our findings indicate that alcohol exposure is associated with altered expression of these genes, which may be relevant to the pathophysiology of AUD.

Indexed as

EthanolGene Expression RegulationGonadotropin-Releasing HormoneHypothalamusSignal TransductionThyroid HormonesAnimalsGene Expression ProfilingGene OntologyMaleMiceMice, Inbred C57BLEthanolGonadotropin-Releasing HormoneThyroid HormonesAlcohol use disorderGnRH signaling pathwayHypothalamusThyroid hormone synthesisTranscriptome sequencing

Identifiers

PMID41057899
PMCPMC12506331

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