Neurological research · 2025
Chronic ethanol exposure alters hypothalamic expression of genes regulating the hypothalamic-pituitary-thyroid axis.
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Huang Zhenghui, Zheng Yifan, Hu Yue, Wang Xiya, Qi Xunzhong, Guo Shubin
Аннотация
BACKGROUND: Chronic alcohol consumption induces persistent neurobiological changes that contribute to cognitive and emotional disturbances. Although the hypothalamus plays a central role in neuroendocrine and emotional regulation, its molecular alterations under chronic alcohol exposure remain poorly understood. This study aimed to characterize transcriptomic changes in the hypothalamus of alcohol-exposed mice and identify the affected signaling pathways.
METHODS: Male mice were subjected to chronic alcohol exposure. Hypothalamic tissues were analyzed via RNA sequencing, followed by KEGG, GO, and Reactome enrichment analyses. Quantitative real-time PCR (qRT-PCR) was performed to validate selected differentially expressed genes.
RESULTS: Transcriptomic profiling and integrative pathway analyses revealed significant differential expression of genes associated with the hypothalamic - pituitary - thyroid (HPT) axis. Notably, Dio2 and Adcy9 were downregulated, while Cga was upregulated in the hypothalamus of alcohol-exposed mice, suggesting a potential disruption in neuroendocrine feedback regulation.
CONCLUSIONS: The altered expression of HPT axis - related genes in the hypothalamus may reflect compensatory neuroendocrine adaptations to chronic alcohol exposure. These findings offer insights into central regulatory mechanisms underlying alcohol-induced hypothalamic dysfunction and provide a basis for further mechanistic studies.
METHODS: Male mice were subjected to chronic alcohol exposure. Hypothalamic tissues were analyzed via RNA sequencing, followed by KEGG, GO, and Reactome enrichment analyses. Quantitative real-time PCR (qRT-PCR) was performed to validate selected differentially expressed genes.
RESULTS: Transcriptomic profiling and integrative pathway analyses revealed significant differential expression of genes associated with the hypothalamic - pituitary - thyroid (HPT) axis. Notably, Dio2 and Adcy9 were downregulated, while Cga was upregulated in the hypothalamus of alcohol-exposed mice, suggesting a potential disruption in neuroendocrine feedback regulation.
CONCLUSIONS: The altered expression of HPT axis - related genes in the hypothalamus may reflect compensatory neuroendocrine adaptations to chronic alcohol exposure. These findings offer insights into central regulatory mechanisms underlying alcohol-induced hypothalamic dysfunction and provide a basis for further mechanistic studies.