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高脂饮食可增强过氧化氢酶加载到脂肪组织衍生的细胞外囊泡中,对氧化应激的影响有限。

High fat diet enhances catalase loading into adipose tissue derived extracellular vesicles with limited effect on oxidative stress.

作者信息

Jeong Inae, Lee Juhwan, Park Soo-Jeung, Kim Ok-Kyung

机构信息

Division of Food and Nutrition, Chonnam National University, Gwangju, 61186, Republic of Korea.

Department of Culinary and Nutrition, Woo-song University, Daejeon, 34606, Republic of Korea.

出版信息

Sci Rep. 2025 Aug 23;15(1):31010. doi: 10.1038/s41598-025-15594-5.

DOI:10.1038/s41598-025-15594-5
PMID:40849334
Abstract

Obesity is closely related to liver disease. However, few studies have focused on the impact of adipose tissue-derived extracellular vesicles (EVs) in obesity on liver disease. Therefore, we aimed to investigate the effect of adipose tissue-derived EVs from high-fat diet (HFD)-fed obese mice (EV-HFD) on liver damage induced by oxidative stress. We investigated alterations in the expression of antioxidant enzymes in adipose tissue, and the loading of those enzymes into adipose tissue-derived EVs. Furthermore, we treated alpha mouse liver 12 (AML12) cells with adipose tissue-derived EVs and induced oxidative stress. We observed that the HFD did not exert an effect on the protein expressions of antioxidant enzymes in adipose tissue. Intriguingly, the EV-HFD exhibited an upregulation in the loading of catalase (CAT) when compared to the adipose tissue-derived EVs from normal chow-fed mice (EV-NC). Notably, both types of EVs exhibited a similar capacity to mitigate cell damage when exposed to oxidative stress. Our findings indicate that obesity-induced loading of more CAT into adipose tissue-derived EVs cannot improve their antioxidant capacity in AML12 cells. We suggest that adipose tissue-derived EVs can serve as a tool to maintain homeostasis and defend against oxidative stress, thereby supporting normal physiological functions.

摘要

肥胖与肝脏疾病密切相关。然而,很少有研究关注肥胖状态下脂肪组织衍生的细胞外囊泡(EVs)对肝脏疾病的影响。因此,我们旨在研究高脂饮食(HFD)喂养的肥胖小鼠脂肪组织衍生的EVs(EV-HFD)对氧化应激诱导的肝损伤的影响。我们研究了脂肪组织中抗氧化酶表达的变化,以及这些酶在脂肪组织衍生的EVs中的装载情况。此外,我们用脂肪组织衍生的EVs处理α小鼠肝脏12(AML12)细胞并诱导氧化应激。我们观察到高脂饮食对脂肪组织中抗氧化酶的蛋白表达没有影响。有趣的是,与正常饮食喂养小鼠的脂肪组织衍生的EVs(EV-NC)相比,EV-HFD中过氧化氢酶(CAT)的装载量上调。值得注意的是,当暴露于氧化应激时,两种类型的EVs减轻细胞损伤的能力相似。我们的研究结果表明,肥胖诱导更多的CAT装载到脂肪组织衍生的EVs中并不能提高其在AML12细胞中的抗氧化能力。我们认为脂肪组织衍生的EVs可以作为维持体内稳态和抵御氧化应激的工具,从而支持正常的生理功能。

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本文引用的文献

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Minimal information for studies of extracellular vesicles (MISEV2023): From basic to advanced approaches.细胞外囊泡研究的最低信息要求(MISEV2023):从基础到先进方法。
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Cellular and exosomal GPx1 are essential for controlling hydrogen peroxide balance and alleviating oxidative stress in hypoxic glioblastoma.细胞内和细胞外的 GPx1 对于控制缺氧性脑胶质瘤中的过氧化氢平衡和缓解氧化应激是必不可少的。
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Overexpression of Mitochondrial Catalase within Adipose Tissue Does Not Confer Systemic Metabolic Protection against Diet-Induced Obesity.
脂肪组织中线粒体过氧化氢酶的过表达并不能赋予对饮食诱导肥胖的全身代谢保护作用。
Antioxidants (Basel). 2023 May 22;12(5):1137. doi: 10.3390/antiox12051137.
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Adipose tissue-derived exosomes contribute to obesity-associated liver diseases in long-term high-fat diet-fed mice, but not in short-term.脂肪组织来源的外泌体在长期高脂饮食喂养的小鼠中会导致肥胖相关的肝脏疾病,但在短期喂养中不会。
Front Nutr. 2023 May 9;10:1162992. doi: 10.3389/fnut.2023.1162992. eCollection 2023.
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Signaling pathways in obesity: mechanisms and therapeutic interventions.肥胖症中的信号通路:机制与治疗干预。
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Role of Adipose Tissue Derived Exosomes in Metabolic Disease.脂肪组织衍生的外泌体在代谢性疾病中的作用。
Front Endocrinol (Lausanne). 2022 May 4;13:873865. doi: 10.3389/fendo.2022.873865. eCollection 2022.
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Therapeutically harnessing extracellular vesicles.治疗性利用细胞外囊泡。
Nat Rev Drug Discov. 2022 May;21(5):379-399. doi: 10.1038/s41573-022-00410-w. Epub 2022 Mar 2.
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Oxidative stress in obesity-associated hepatocellular carcinoma: sources, signaling and therapeutic challenges.肥胖相关肝细胞癌中的氧化应激:来源、信号转导和治疗挑战。
Oncogene. 2021 Aug;40(33):5155-5167. doi: 10.1038/s41388-021-01950-y. Epub 2021 Jul 21.
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