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Obesity and weight loss could alter the properties ofadipose stem cells？

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Obesity and weight loss could alter the properties of adipose stem cells?

Leandra S Baptista, Karina R Silva, Radovan BorojevicLeandra S Baptista, Radovan Borojevic, Laboratório de bioengenharia de tecidos, Instituto Nacional de Metrologia, Qualidade e Tecnologia (Inmetro), Duque de Caxias 25250-020, Brazil Leandra S Baptista, Núcleo Multidisciplinar de Pesquisa em Xerém (Numpex-Bio), Universidade Federal do Rio de Janeiro (UFRJ), Campus de Xerém, Rio de Janeiro 21941-590, BrazilKarina R Silva, Radovan Borojevic, Programa de Pós-graduação em Clínica Médica, Universidade Federal do Rio de Janeiro (UFRJ), Hospital Universitário Clementino Fraga Filho (HUCFF), Rio de Janeiro 21941-590, Brazil Author contributions: Baptista LS and Borojevic R substantially contributed to the concept of the review and finalized the text; Baptista LS and Silva KR contributed to the text and designed the images. Supported by Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ); Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/Correspondence to: Leandra S Baptista, PhD, Laboratório de bioengenharia de tecidos, Instituto Nacional de Metrologia, Qualidade e Tecnologia (Inmetro), Av. Nossa Senhora das Graças, 50 - Xerém, Duque de Caxias 25250-020, Brazil. leandra.baptista@gmail.comTelephone: +55-21-26799834Fax: +55-21-26799837Received: July 26, 2014 Peer-review started: July 26, 2014First decision: August 28, 2014Revised: September 22, 2014Accepted: October 23, 2014Article in press: December 16, 2014Published online: January 26, 2015

Abstract The discovery that adipose tissue represents an

interesting source of multipotent stem cells has led to many studies exploring the clinical potential of these cells in cell-based therapies. Recent advances in understanding the secretory capacity of adipose tissue and the role of adipokines in the development of obesity and associated disorders have added a new dimension to the study of adipose tissue biology in normal and diseased states. Subcutaneous adipose tissue forms the interface between the clinical application of regenerative medicine and the establishment of the pathological condition of obesity. These two facets of adipose tissue should be understood as potentially related phenomena. Because of the functional characteristics of adipose stem cells, these cells represent a fundamental tool for understanding how these two facets are interconnected and could be important for therapeutic applications. In fact, adipose tissue stem cells have multiple functions in obesity related to adipogenic, angiogenic and secretory capacities. In addition, we have also previously described a predominance of larger blood vessels and an adipogenic memory in the subcutaneous adipose tissue after massive weight loss subsequent to bariatric surgery (ex-obese patients). Understanding the reversibility of the behavior of adipose stem cells in obeses and in weight loss is relevant to both physiological studies and the potential use of these cells in regenerative medicine.

Key words: Adipose stem cells; Subcutaneousadipose

tissue; Obesity; Weight loss; Regenerative medicine

© The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.

Core tip: In this mini-review, we summarize recent

aspects regarding obese subcutaneous adipose tissue with a focus in adipogenic and secretory capacities of adipose stem cells. In particular, we discuss how the occurrence of obesity and weight loss could alter the properties of stem cells and the consequences of using adipose-derived stem cells in regenerative medicine.

MINIREVIEWSSubmit a Manuscript: http://www.wjgnet.com/esps/Help Desk: http://www.wjgnet.com/esps/helpdesk.aspxDOI: 10.4252/wjsc.v7.i1.165World J Stem Cells 2015 January 26; 7(1): 165-173ISSN 1948-0210 (online)© 2015 Baishideng Publishing Group Inc. All rights reserved.

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obesity

obesity


Key words: obesity, causes, effect, measures
1. The introduction of obesity

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have a negative effect on health, leading to reduced life expectancy or increased health problems.
2. The causes of obesity

Obesity is most commonly caused by a combination of excessive food energy intake, lack of physical activity, and genetic susceptibility, and a few cases are caused primarily by hormone imbalance and psychological factors.
References

[1]Pool, Robert (2001). Fat: Fighting the Obesity Epidemic. Oxford, UK: Oxford University Press. ISBN 0-19-511853-7. [2]Kiperman, Peter G; Cater son, Ian D.; Dietz, William H., eds. (2009). Clinical obesity in Adults and Children (3rd Ed.). John Wiley & Sons. ISBN 978-1-4443-0763-4. [3] Foment, Michael (1997). The Fat of the Land: Our Health Crises and How Overweight Americans can Help Themselves. New York: Penguin Books. ISBN 0-14026144-3. [4] Keller, Kathleen (2008). Encyclopedia of Obesity. Thousand Oaks, Caliph: Sage Publications, Inc. ISBN 1-4129-5238-7. [5] Levy-Navarro, Elena (2008). The Culture of Obesity in Early and Late Modernity. Palgrave Macmillan. ISBN 0-230-60123-5.
文档：免疫代谢

文档：免疫代谢

免疫代谢免疫代谢（immunometabolism）主要研究免疫与代谢及其两者之间的密切转化关系，包括两个方面：1）免疫细胞在器官代谢和代谢疾病中的作用，2）免疫细胞内发生的代谢过程及其如何影响整体免疫力生物体的代谢可以影响淋巴细胞的生理和活性。

通过释放炎性细胞因子，CD4 + T辅助细胞（特别是Th1和Th17）是促炎症环境的主要介质之一，而Treg细胞为直接负责抑制Th1和Th17细胞对应物的作用, ，从而协调T细胞体内平衡和抑制自身反应。

在自身免疫性疾病发展的中心核心，Th1 / Th17和Treg细胞之间的平衡受到破坏，Treg 变得有缺陷，Th1 / Th17细胞异常活化。

慢性低度炎症是驱动许多常见慢性疾病，如肥胖、胰岛素抵抗和癌症，的代谢并发症的主要因素。

完整的炎症通路对于组织的健康和适当的体内平衡是至关重要的。

因此，炎症途径的普遍破坏不仅可以抵御入侵者的能力，而且还会导致组织损伤，甚至通过破坏修复和重塑或通过产生失语症引起全身性炎症。

, 通过大量的研究，已经对免疫细胞的代谢有了初步的了解。

接受T细胞受体（TCR）和共刺激信号后，T细胞会生长、扩增，并最终分化成不同的细胞毒性T细胞，Treg和辅助T 细胞（Th细胞，即Th1、Th2和Th17）, 。

除了一些已知的级联反应信号，代谢活性的变化与T细胞分化和效应功能密切相关。

初始T细胞依赖氧化磷酸化（OXOPHOS）维持能源需求;相反，活化的T细胞通过有氧糖酵解消耗大量的葡萄糖。

阻断糖酵解或降低T细胞活化期间的葡萄糖摄取可以降低T细胞活化，Th细胞分化，以及细胞因子的产生，包括IFNγ、IL-2和Th1细胞中的IL-17a。

相反，通过过表达T细胞中的葡萄糖转运蛋白1（GLUT1）会提高细胞的糖酵解总量，增强小鼠的炎症反应。

当通过调节关键酶如丙酮酸激酶M2（PKM2）抑制糖酵解时，巨噬细胞会向更多M2状态的转变，例如IL-10生产。

在Th17中观察到类似的效应，如果糖酵解被2-脱氧葡萄糖抑制或如果缺氧诱导因子-1a（HIF-1a）被消融，则其变得更像Treg细胞。

袖状胃切除和Roux-en-Y胃旁路手术后贫血的发生原因和预防策略

袖状胃切除和Roux-en-Y胃旁路手术后贫血的发生原因和预防策略

Journal of Minimall y Invasive Medicine,2021,16(1)・1・-微创医学技术前沿・袖状胃切除和Roux-en-Y胃旁路手术后贫血的发生原因和预防策略董志勇陈国骥胡瑞翔姜舒文陈文辉王存川(暨南大学附属第一医院胃肠外科,广东省广州市510630)董志勇，医学博士、副主任医师、硕士研究生导师，现任暨南大学附属第一医院(广州)胃肠外科副主任医师、肥胖代谢外科主任,为美国西北大学访问学者、国际肥胖与代谢病外科联盟(IFSO)会员,从事肥胖与代谢外科、胃肠外科、腹壁疝外科临床及科研工作10余年，是最先提出"三孔七步法袖状胃切除术”和"基于膜解剖的腹腔镜袖状胃切除术”概念的减重外科医生。

发表肥胖与代谢外科和胃肠肿瘤外科相关中英文论文50多篇，其中作为第一作者发表SCI论文13篇，作为通信作者发表SCI论文3篇。

主持广东省自然科学基金1项、广东省卫生厅科学基金1项、暨南大学人才引进科研项目1项，参与国家自然科学基金课题研究2项【关键词】Roux-en-Y胃旁路术;袖状胃切除术;贫血;减重手术【中图分类号】R656.6+1【文献标识码】A【文章编号】1673-6575(2021)01-0001-05D0I：10.11864/j.issn.1673.2021.01.01随着经济社会的快速发展和生活方式的巨大改变，肥胖症的发病率在世界范围内越来越高，肥胖还会引起肥胖相关的代谢并发症［1］(我国成年人肥胖率已超过10%,且有进一步增长的趋势［2］。

循证医学证，重肥胖，减重手术有良的减重，还疗2型糖尿病，具有缓解相关代谢疾病等［3］(2018年国际肥胖与代谢病外科⑷,已有38.2%的肥胖患者接受Roux-en-Y胃旁路术(Roux-en-Y gastric bypas s,RYGB),46.0%的肥胖患袖状胃切除术(sleeve gastrectomy,SG)。

组蛋白甲基化与脂肪生成

组蛋白甲基化与脂肪生成

组蛋白甲基化与脂肪形成摘要最近的研究表明，在脂肪形成过程中，很多基因的表达受到表观遗传的调控。

组蛋白甲基化是一种重要的表观遗传学修饰，人们对其已经进行了深入的研究。

组蛋白甲基化可以通过调控脂肪细胞分化过程中转录因子及脂肪组织特异性基因的表达，从而调控脂肪组织的形成。

该文综述了脂肪形成过程中组蛋白甲基化及去甲基化表观调控的最新进展，探讨了脂肪组织组蛋白甲基化的研究趋势和未来发展方向。

关键词组蛋白甲基化；脂肪形成；基因表达；组蛋白甲基转移酶；组蛋白去甲基化酶随着经济的不断发展，肥胖已经成为全球性的公共健康问题，Ⅱ型糖尿病的发生占所有糖尿病的90%-95%，肥胖是Ⅱ型糖尿病的首要危险因素；肥胖还能增加某些类型癌症的发病风险，包括乳腺癌、肾癌、卵巢癌、胰腺癌、前列腺癌、肝癌、大肠癌、黑色素瘤等(1)；最近有研究表明肥胖可加速人类肝脏的衰老(2)。

研究脂肪形成的分子机制将为治疗与糖尿病密切相关的肥胖和脂代谢障碍疾病等提供重要理论依据。

组蛋白甲基化可以通过调控脂肪细胞分化过程中转录因子及脂肪组织特异性基因的表达，从而在脂肪形成过程中发挥着重要作用。

1 组蛋白甲基化组蛋白甲基化作为一种重要的表观遗传学修饰方式，与基因转录调控、异染色质的形成、X染色体失活，基因组印记等密切相关。

(3)组蛋白甲基化的异常与多种人类疾病如肿瘤的发生等相关(4)。

与乙酰化不同，组蛋白甲基化对基因表达调控的作用可以完全相反，有时促进基因表达，有时却抑制基因表达，调控作用取决于甲基化的位点和甲基化的程度。

如H3K4甲基化与基因激活有关，而H3K9和H3K27甲基化与基因沉默相关(3, 5)。

组蛋白的甲基化修饰是由一类含有SET结构域、被称为组蛋白甲基转移酶（HMTs）的蛋白质来催化的。

SET结构域由最早发现表达这三个结构域的3个基因来命名，分别为Su(var)3−9, Enhancer of zeste (E(z))和trithorax (trx)(6)。