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肥胖与非肥胖个体间脂质体脂质的比较

Comparison of Adiposomal Lipids between Obese and Non-Obese Individuals.

作者信息

Hussein Mohamed, Mirza Imaduddin, Morsy Mohammed, Mostafa Amro, Hassan Chandra, Masrur Mario, Bianco Francesco M, Papasani Subbaiah, Levitan Irena, Mahmoud Abeer M

机构信息

Department of Pathology, University of Kentucky, Lexington, KY 40536, USA.

Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA.

出版信息

Metabolites. 2024 Aug 21;14(8):464. doi: 10.3390/metabo14080464.

DOI:10.3390/metabo14080464
PMID:39195560
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11356626/
Abstract

Our recent findings revealed that human adipose tissues (AT)-derived extracellular vesicles (adiposomes) vary in cargo among obese and lean individuals. The main objective of this study was to investigate the adiposomal lipid profiles and their correlation with cardiometabolic risk factors. AT samples were collected from obese subjects and lean controls and analyzed for their characteristics and lipid content. In addition, we measured the correlation between adiposomal lipid profiles and body composition, glucose and lipid metabolic profiles, brachial artery vasoreactivity, AT arteriolar flow-induced dilation, and circulating markers such as IL-6, C-reactive protein, and nitric oxide (NO). Compared to lean controls, adiposomes isolated from obese subjects were higher in number after normalization to AT volume. The two major lipid classes differentially expressed were lysophosphatidylcholine/phosphatidylcholine (LPC/PC) and ceramides (Cer). All lipids in the LPC/PC class were several-fold lower in adiposomes from obese subjects compared to lean controls, on top of which were PC 18:2, PC 18:1, and PC 36:3. Most ceramides were markedly upregulated in the obese group, especially Cer d37:0, Cer d18:0, and Cer d39:0. Regression analyses revealed associations between adiposomal lipid profiles and several cardiometabolic risk factors such as body mass index (BMI), fat percentage, insulin resistance, arteriolar and brachial artery vasoreactivity, NO bioavailability, and high-density lipoproteins (HDL-C). We conclude that the ability of adiposomes from obese subjects to disrupt cardiometabolic function could be partly attributed to the dysregulated lipid cargo.

摘要

我们最近的研究结果显示,人类脂肪组织(AT)衍生的细胞外囊泡(脂肪体)在肥胖个体和瘦个体中的货物成分存在差异。本研究的主要目的是调查脂肪体的脂质谱及其与心脏代谢危险因素的相关性。从肥胖受试者和瘦对照组收集AT样本,并分析其特征和脂质含量。此外,我们测量了脂肪体脂质谱与身体成分、葡萄糖和脂质代谢谱、肱动脉血管反应性、AT小动脉血流诱导的扩张以及循环标志物如白细胞介素-6、C反应蛋白和一氧化氮(NO)之间的相关性。与瘦对照组相比,从肥胖受试者中分离出的脂肪体在以AT体积标准化后数量更多。差异表达的两种主要脂质类别是溶血磷脂酰胆碱/磷脂酰胆碱(LPC/PC)和神经酰胺(Cer)。与瘦对照组相比,肥胖受试者脂肪体中LPC/PC类的所有脂质均低几倍,其中PC 18:2、PC 18:1和PC 36:3含量最低。大多数神经酰胺在肥胖组中显著上调,尤其是Cer d37:0、Cer d18:0和Cer d39:0。回归分析揭示了脂肪体脂质谱与几种心脏代谢危险因素之间的关联,如体重指数(BMI)、脂肪百分比、胰岛素抵抗、小动脉和肱动脉血管反应性、NO生物利用度以及高密度脂蛋白(HDL-C)。我们得出结论,肥胖受试者的脂肪体破坏心脏代谢功能的能力可能部分归因于脂质货物失调。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/d4fd51589142/metabolites-14-00464-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/ca59b920b030/metabolites-14-00464-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/775b14c05556/metabolites-14-00464-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/00c5a9f5b6b5/metabolites-14-00464-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/e4659516c987/metabolites-14-00464-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/87e2a0e680aa/metabolites-14-00464-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/8fa8b76ec01e/metabolites-14-00464-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/7985752e1a4c/metabolites-14-00464-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/d4fd51589142/metabolites-14-00464-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/ca59b920b030/metabolites-14-00464-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/775b14c05556/metabolites-14-00464-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/00c5a9f5b6b5/metabolites-14-00464-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/e4659516c987/metabolites-14-00464-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/87e2a0e680aa/metabolites-14-00464-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/8fa8b76ec01e/metabolites-14-00464-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/7985752e1a4c/metabolites-14-00464-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c7f/11356626/d4fd51589142/metabolites-14-00464-g008.jpg

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本文引用的文献

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Cells. 2023 Oct 15;12(20):2453. doi: 10.3390/cells12202453.
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