线粒体rRNA单倍型变异易患代谢综合征-动脉网

Haplotype variability in mitochondrial rRNA predisposes to metabolic syndrome

Nature 等信源发布 2024-09-11 18:45

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AbstractMetabolic syndrome is a growing concern in developed societies and due to its polygenic nature, the genetic component is only slowly being elucidated. Common mitochondrial DNA sequence variants have been associated with symptoms of metabolic syndrome and may, therefore, be relevant players in the genetics of metabolic syndrome.

。常见的线粒体DNA序列变异与代谢综合征的症状有关，因此可能是代谢综合征遗传学的相关参与者。

We investigate the effect of mitochondrial sequence variation on the metabolic phenotype in conplastic rat strains with identical nuclear but unique mitochondrial genomes, challenged by high-fat diet. We find that the variation in mitochondrial rRNA sequence represents risk factor in the insulin resistance development, which is associated with diacylglycerols accumulation, induced by tissue-specific reduction of the oxidative capacity.

我们研究了线粒体序列变异对高脂饮食挑战的具有相同核但独特线粒体基因组的conplastic大鼠品系代谢表型的影响。我们发现线粒体rRNA序列的变化代表了胰岛素抵抗发展的危险因素，这与组织特异性氧化能力降低引起的甘油二酯积累有关。

These metabolic perturbations stem from the 12S rRNA sequence variation affecting mitochondrial ribosome assembly and translation. Our work demonstrates that physiological variation in mitochondrial rRNA might represent a relevant underlying factor in the progression of metabolic syndrome..

这些代谢扰动源于影响线粒体核糖体组装和翻译的12S rRNA序列变异。我们的工作表明，线粒体rRNA的生理变异可能是代谢综合征进展的相关潜在因素。。

IntroductionMitochondria, the organelles of bacterial origin, still maintain mitochondrial DNA (mtDNA), and its sequence exerts variability (single nucleotide polymorphisms – SNPs), dividing the population into mtDNA families known as haplogroups1. Unlike nuclear DNA (nDNA), mtDNA in mammals is maternally inherited and encodes only 13 structural proteins, the subunits of the oxidative phosphorylation apparatus (OXPHOS), two ribosomal RNAs and 22 transfer RNAs required for mitochondrial protein synthesis.

引言线粒体是细菌起源的细胞器，仍然维持线粒体DNA（mtDNA），其序列具有变异性（单核苷酸多态性–SNP），将种群划分为称为单倍群的mtDNA家族1。与核DNA（nDNA）不同，哺乳动物中的mtDNA是母体遗传的，仅编码13种结构蛋白，氧化磷酸化装置（OXPHOS）的亚基，线粒体蛋白合成所需的两个核糖体RNA和22种转移RNA。

The nuclear genome encodes the remaining more than 1000 mitochondrial proteins, which are transported into the mitochondria2. This requires coordination in expression and translation between the two genomes3,4. Recently, studies in human populations have associated mtDNA haplogroups with the risk of metabolic syndrome or its complications5,6,7, and sequence variation in mtDNA has also been shown to influence the expression of stress response genes8.A higher risk of metabolic syndrome is strongly associated with weight gain due to high nutrient excess9.

核基因组编码剩余的1000多种线粒体蛋白，这些蛋白被转运到线粒体2中。这需要两个基因组之间的表达和翻译协调3,4。。

The resulting aberrant distribution of fat, mainly in visceral and intra-abdominal depots10,11, leads to lipotoxicity—ectopic fat storage in metabolically active tissues such as the liver, myocardium, or skeletal muscle12. The metabolic disbalance is associated with symptoms such as insulin resistance, type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease, or cardiovascular disease13.While the link between mitochondrial function and metabolic syndrome is widely accepted, the molecular mechanisms behind it still need to be better defined.

由此产生的脂肪异常分布，主要在内脏和腹腔内储存10,11，导致脂肪毒性异位脂肪储存在代谢活跃的组织如肝脏，心肌或骨骼肌12。代谢失衡与胰岛素抵抗，2型糖尿病（T2DM），非酒精性脂肪肝或心血管疾病等症状有关13。虽然线粒体功能与代谢综合征之间的联系已被广泛接受，但其背后的分子机制仍需要更好地定义。

Many studies have associated insulin resistance and T2DM with a decrease in mitochondrial oxidative capacity14,15, which results in the inefficient fatty acid oxidation. Subs.

许多研究将胰岛素抵抗和T2DM与线粒体氧化能力降低联系起来[14,15]，这导致脂肪酸氧化效率低下。。

Data availability

数据可用性

The published article and its supplementary information include all data generated and analysed in the study. Uncropped and unedited western blot images are provided in the Supplementary information as Supplementary Fig. 9. A complete source data file is provided as Supplementary Data. Label-free quantification mass spectrometry (LFQ-MS) data have been deposited at PRIDE and are publicly available (accession numbers: PXD045910 and PXD052976)..

已发表的文章及其补充信息包括研究中产生和分析的所有数据。补充信息中提供了未剪切和未编辑的蛋白质印迹图像作为补充图9。完整的源数据文件作为补充数据提供。无标记定量质谱（LFQ-MS）数据已保存在PRIDE，并可公开获得（登录号：PXD045910和PXD052976）。。

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Download referencesAcknowledgementsThis work was supported by the Czech Science Foundation GACR 19-10354S (P.P., V.K., G.P.-F., J.S., J.H., and A.P.), the National Institute for Research of Metabolic and Cardiovascular Diseases (Programme EXCELES, ID Project No. LX22NPO5104)—Funded by the European Union-Next Generation EU (K.T., T.M.

下载参考文献致谢这项工作得到了捷克科学基金会GACR 19-10354S（P.P.，V.K.，G.P.-F.，J.S.，J.H。和A.P.）的支持，国家代谢和心血管疾病研究所（计划EXCELES，ID项目号LX22NPO5104）由欧盟下一代欧盟（K.T.，T.M.）资助。

and S.K.), and by the grant LUAUS23095 within the INTER-EXCELLENCE program of the Ministry of Education, Youth, and Sports of the Czech Republic (M.P.). O.G. was supported by the project P JAC CZ.02.01.01/00/22_008/0004575 RNA for therapy, Co-Funded by the European Union. The authors would like to acknowledge the Laboratory of Metabolomics at the Institute of Physiology of the Czech Academy of Sciences (T.C.) and the Proteomics Service Laboratory at the Institute of Physiology (supported by RVO, ID 67985823) and the Institute of Molecular Genetics (supported by RVO, ID 68378050) of the Czech Academy of Sciences (M.V.).

和S.K.），以及捷克共和国教育、青年和体育部（M.P.）卓越计划内的LUAUS23095赠款。O、 G.得到了欧盟共同资助的P JAC CZ.02.01.01/00/22\U 008/0004575 RNA治疗项目的支持。作者要感谢捷克科学院生理学研究所代谢组学实验室和生理学研究所蛋白质组学服务实验室（由RVO支持，ID 67985823）和分子遗传学研究所（由RVO支持，ID 68378050）捷克科学院（M.V.）。

The National Center for Medical Genomics (LM2023067) kindly provided WGS sequencing (S.K., V.S.). Graphical abstract and Figs. 1a and 5a were created with BioRender.com.Author informationAuthors and AffiliationsLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech RepublicPetr Pecina, Kristýna Čunátová, Vilma Kaplanová, Guillermo Puertas-Frias, Kateřina Tauchmannová, Marek Vrbacký, Josef Houštěk, Tomáš Mráček & Alena PecinováLaboratory of Genetics of Model Diseases, Institute of Physiology, Czech Academy of Sciences, Prague, Czech RepublicJan Šilhavý & Michal PravenecLaboratory of Translational Metabolism, Institute of Physiology, Czech Academy of Sciences, Prague, Czech RepublicTomáš ČajkaInstitute of Parasitology, Biology Centre, Czech Academy of Sciences, České Buděj.

国家医学基因组学中心（LM2023067）提供了WGS测序（S.K.，V.S.）。图形摘要和图1a和5a由BioRender.com创建。作者信息作者和附属机构捷克科学院生理学研究所生物能学实验室，捷克共和国布拉格Petr Pecina、KristýnaČunátová、Vilma Kaplanová、Guillermo Puertas Frias、Kateřina Tauchmannová、Marek Vrbacký、Josef Houstěk、TomášMráček

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PubMed Google ScholarContributionsConceptualization, J.H., T.M., and A.P.; Methodology, P.P., M.P, T.M., and A.P.; Formal analysis, M.V., T.C., O.G., and V.S.; Investigation, P.P., K.C., V.K., G.P.-F., J.S., V.S., S.K., T.M., and A.P.; Resources, M.H., M.P., T.C., and M.V., Writing—Original draft, J.H., T.M., and A.P.; Writing—Review & Editing, P.P., K.C., V.K., K.T., M.V., T.C., O.G., M.P., J.H., T.M., and A.P.; Visualization, T.M.

PubMed谷歌学术贡献概念化，J.H.，T.M。和A.P。；方法论，P.P.，M.P，T.M。和A.P。；形式分析，M.V.，T.C.，O.G。和V.S。；调查，P.P.，K.C.，V.K.，G.P.-F.，J.S.，V.S.，S.K.，T.M。和A.P。；资源，M.H.，M.P.，T.C。和M.V.，撰写原稿，J.H.，T.M。和A.P。；写作评论与编辑，P.P.，K.C.，V.K.，K.T.，M.V.，T.C.，O.G.，M.P.，J.H.，T.M。和A.P。；可视化，T.M。

and A.P.; Funding acquisition, O.G., M.P., T.M., and A.P.Corresponding authorsCorrespondence to.

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Reprints and permissionsAbout this articleCite this articlePecina, P., Čunátová, K., Kaplanová, V. et al. Haplotype variability in mitochondrial rRNA predisposes to metabolic syndrome.

转载和许可关于这篇文章引用这篇文章Pecina，P.，Čunátová，K.，Kaplanová，V.等人。线粒体rRNA的单倍型变异易患代谢综合征。

Commun Biol 7, 1116 (2024). https://doi.org/10.1038/s42003-024-06819-wDownload citationReceived: 19 December 2023Accepted: 30 August 2024Published: 11 September 2024DOI: https://doi.org/10.1038/s42003-024-06819-wShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

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