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低氧诱导因子-3α/过氧化物酶体增殖物激活受体-γ通过改变团头鲂的糖酵解和脂质合成来调节低氧耐受性

HIF-3α/PPAR-γ Regulates Hypoxia Tolerance by Altering Glycolysis and Lipid Synthesis in Blunt Snout Bream ().

作者信息

Jiang Minggui, Huang Jing, Guo Xing, Fu Wen, Peng Liangyue, Wang Yang, Liu Wenbin, Liu Jinhui, Zhou Li, Xiao Yamei

机构信息

College of Life Sciences, Hunan Normal University, Changsha 410081, China.

Engineering Research Center of Polyploid Fish Reproduction and Breeding of the State Education Ministry, Changsha 410081, China.

出版信息

Int J Mol Sci. 2025 Mar 14;26(6):2613. doi: 10.3390/ijms26062613.

Abstract

Hypoxic stress causes cell damage and serious diseases in organisms, especially in aquatic animals. It is important to elucidate the changes in metabolic function caused by hypoxia and the mechanisms underlying these changes. This study focuses on the low oxygen tolerance feature of a new blunt snout bream strain (GBSBF1). Our data show that GBSBF1 has a different lipid and carbohydrate metabolism pattern than wild-type bream, with altering glycolysis and lipid synthesis. In GBSBF1, the expression levels of and genes are significantly decreased, while the activation of HIF-3α protein is observed to have risen significantly. The results indicate that enhanced HIF-3α can positively regulate gpd1ab and gpam through PPAR-γ, which increases glucose metabolism and reduces lipolysis of GBSBF1. This research is beneficial for creating new aquaculture strains with low oxygen tolerance traits.

摘要

低氧应激会导致生物体,尤其是水生动物的细胞损伤和严重疾病。阐明缺氧引起的代谢功能变化及其背后的机制非常重要。本研究聚焦于一种新的团头鲂品系(GBSBF1)的低氧耐受特性。我们的数据表明,GBSBF1与野生型团头鲂具有不同的脂质和碳水化合物代谢模式,糖酵解和脂质合成发生改变。在GBSBF1中, 和 基因的表达水平显著降低,而HIF-3α蛋白的激活则显著升高。结果表明,增强的HIF-3α可通过PPAR-γ正向调节gpd1ab和gpam,从而增加GBSBF1的葡萄糖代谢并减少脂肪分解。本研究有助于培育具有低氧耐受特性的新型水产养殖品系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9679/11942064/5a2f0a8b214c/ijms-26-02613-g001.jpg

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