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人体急性冲刺运动后脂肪组织中线粒体相关基因表达降低:一项初步研究。

Decreased mitochondrial-related gene expression in adipose tissue after acute sprint exercise in humans: A pilot study.

机构信息

Division of Clinical Physiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.

Unit of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.

出版信息

Physiol Rep. 2024 Oct;12(20):e70088. doi: 10.14814/phy2.70088.

DOI:10.14814/phy2.70088
PMID:39431556
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11492148/
Abstract

The aim was to examine the acute effects of sprint exercise (SIT) on global gene expression in subcutaneous adipose tissue (AT) in healthy subjects, to enhance understanding of how SIT influences body weight regulation. The hypothesis was that SIT upregulates genes involved in mitochondrial function and fat metabolism. A total of 15 subjects performed three 30-s all-out sprints (SIT). Samples were collected from AT, skeletal muscle (SM) and blood (brachial artery and a subcutaneous AT vein) up to 15 min after the last sprint. Results showed that markers of oxidative stress, such as the purines hypoxanthine, xanthine and uric acid, increased markedly by SIT in both the artery and the AT vein. Purines also increased in AT and SM tissue. Differential gene expression analysis indicated a decrease in signaling for mitochondrial-related pathways, including oxidative phosphorylation, electron transport, ATP synthesis, and heat production by uncoupling proteins, as well as mitochondrial fatty acid beta oxidation. This downregulation of genes related to oxidative metabolism suggests an early-stage inhibition of the mitochondria, potentially as a protective mechanism against SIT-induced oxidative stress.

摘要

目的是研究急性冲刺运动(SIT)对健康受试者皮下脂肪组织(AT)整体基因表达的影响,以增强对 SIT 如何影响体重调节的理解。假设是 SIT 会上调与线粒体功能和脂肪代谢相关的基因。共有 15 名受试者进行了三次 30 秒的全力冲刺(SIT)。最后一次冲刺后 15 分钟内,从 AT、骨骼肌(SM)和血液(肱动脉和皮下 AT 静脉)采集样本。结果表明,SIT 会使动脉和 AT 静脉中的嘌呤(如次黄嘌呤、黄嘌呤和尿酸)等氧化应激标志物显著增加。嘌呤也在 AT 和 SM 组织中增加。差异基因表达分析表明,与氧化代谢相关的信号通路(包括氧化磷酸化、电子传递、ATP 合成和解偶联蛋白的产热)以及线粒体脂肪酸β氧化的相关基因表达下调。这种与氧化代谢相关的基因下调表明,线粒体早期受到抑制,可能是一种针对 SIT 诱导的氧化应激的保护机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/a2e23ac69b41/PHY2-12-e70088-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/0003236220b7/PHY2-12-e70088-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/30175930c7b6/PHY2-12-e70088-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/7d7f78d4aba3/PHY2-12-e70088-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/d12fc0886232/PHY2-12-e70088-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/ab21b93221c0/PHY2-12-e70088-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/a2e23ac69b41/PHY2-12-e70088-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/0003236220b7/PHY2-12-e70088-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/30175930c7b6/PHY2-12-e70088-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/7d7f78d4aba3/PHY2-12-e70088-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/d12fc0886232/PHY2-12-e70088-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/ab21b93221c0/PHY2-12-e70088-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5921/11492148/a2e23ac69b41/PHY2-12-e70088-g003.jpg

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