切换至 "中华医学电子期刊资源库"

中华肥胖与代谢病电子杂志 ›› 2021, Vol. 07 ›› Issue (04) : 260 -265. doi: 10.3877/cma.j.issn.2095-9605.2021.04.008

综述

不同组织慢性炎症的特点及其在胰岛素抵抗发展中的作用
于莉莉1, 李艳花1, 张朝阳1, 邓一鸣1, 林剑泷1, 冯志伟1,()   
  1. 1. 453003 新乡,新乡医学院基础医学院免疫学系
  • 收稿日期:2021-06-26 出版日期:2021-11-30
  • 通信作者: 冯志伟
  • 基金资助:
    国家自然科学基金(81500675、82070895); 2020年大学生创新创业训练计划项目(S202010472059); 新乡医学院基础医学院培育项目(JCYXYKY202023)

Characteristics of chronic inflammation in different tissues and their effects on insulin resistance

Lili Yu1, Yanhua Li1, Chaoyang Zhang1   

  • Received:2021-06-26 Published:2021-11-30
引用本文:

于莉莉, 李艳花, 张朝阳, 邓一鸣, 林剑泷, 冯志伟. 不同组织慢性炎症的特点及其在胰岛素抵抗发展中的作用[J]. 中华肥胖与代谢病电子杂志, 2021, 07(04): 260-265.

Lili Yu, Yanhua Li, Chaoyang Zhang. Characteristics of chronic inflammation in different tissues and their effects on insulin resistance[J]. Chinese Journal of Obesity and Metabolic Diseases(Electronic Edition), 2021, 07(04): 260-265.

图1 肥胖诱导的组织慢性炎症 注:肥胖可以引起组织慢性炎症状态,是胰岛素抵抗和T2DM的主要诱因。肥胖诱导的慢性炎症对脂肪组织,肌肉,肝脏,胰岛和肠道产生了一系列影响,这些炎症状态改变包括免疫细胞的浸润和细胞因子的分泌等,是肥胖相关代谢性疾病发生和发展的关键
图2 肥胖慢性炎症的自我反馈过程 注:肥胖会导致内质网应激、缺氧、脂毒性、菌群失调及激素紊乱,进而启动实质细胞内促炎症途径的激活(第一步)。在实质细胞激活后,它们分泌的多种趋化因子(第二步),引起巨噬细胞的趋化和迁移以及其他免疫细胞浸润组织中(第三步)。这些免疫细跑具有促炎作用,分泌多种因子,包括细胞因子及代谢组织循环中其他信号分子等,并通过局部旁分泌作用,导致脂肪细胞、肝细胞、肌细胞产生胰岛素抵抗和β细胞内GSIS下降,最终产生T2DM(第四步)
[1]
Rebuffat SA, Sidot E, Guzman C, et al. Adipose tissue derived-factors impaired pancreatic β-cell function in diabetes [J]. Biochimica et Biophysica Acta Molecular Basis of Disease, 2018, 1864(10): 3378-3387.
[2]
Yue T, Xu S, Huang LL, et al. Obesity and insulin resistance: Pathophysiology and treatment [J]. Drug Discovery Today, 2021, 11(01): 10-16..
[3]
Michailidou Z, Gomez-Salazar M, Alexaki VI. Innate Immune Cells in the Adipose Tissue in Health and Metabolic Disease [J]. Journal of Innate Immunity, 2022, 14(1): 4-30.
[4]
Yu LL, Li YH, Du CC, et al. Pattern Recognition Receptor-Mediated Chronic Inflammation in the Development and Progression of Obesity-Related Metabolic Diseases [J]. Mediators of Inflammation, 2019, 2019: 5271295.
[5]
Chung KJ, Nati M, Chavakis T, et al. Innate immune cells in the adipose tissue [J]. Reviews in endocrine & Metabolic Disorders, 2018, 19(4): 283-292.
[6]
Lumeng CN, Bodzin JL, Saltiel AR. Obesity induces a phenotypic switch in adipose tissue macrophage polarization [J]. Journal of Clinical Investigation, 2007, 117(1): 175-184.
[7]
Sica A, Mantovani A. Macrophage plasticity and polarization: in vivo veritas [J]. Journal of Clinical Investigation, 2012, 122(3): 787-795.
[8]
Lackey DE, Olefsky JM. Regulation of metabolism by the innate immune system [J]. Nature Reviews Endocrinology, 2016, 12(1): 15-28.
[9]
Hotamisligil GS. Inflammation, metaflammation and immunometabolic disorders [J]. Nature, 2017, 542(7640): 177-185.
[10]
Nussbaum JC, Van-Dyken SJ, Moltke J, et al. Type 2 innate lymphoid cells control eosinophil homeostasis [J]. Nature, 2013, 502(7470): 245-248.
[11]
Talukdar S, Oh DY, Bandyopadhyay G, et al. Neutrophils mediate insulin resistance in mice fed a high-fat diet through secreted elastase [J]. Nature Medicine, 2012, 18(9): 1407-1412.
[12]
Zatterale F, Longo M, Naderi J, et al. Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes [J]. Frontiers in Physiology, 2019, 10: 1607.
[13]
Wang Q, Wu HZ. T Cells in Adipose Tissue: Critical Players in Immunometabolism[J]. Frontiers in Immunology, 2018, 9: 2509.
[14]
Bapat SP, Myoung-Suh J, Fang S, et al. Depletion of fat-resident Treg cells prevents age-associated insulin resistance [J]. Nature, 2015, 528(7580): 137-141.
[15]
McLaughlin T, Liu LF, Lamendola C, et al. T-cell profile in adipose tissue is associated with insulin resistance and systemic inflammation in humans [J]. Arteriosclerosis, Thrombosis, and Vascular Biology, 2014, 34(12): 2637-2643.
[16]
Gola A, Dorrington MG, Speranza E, et al. Commensal-driven immune zonation of the liver promotes host defence [J]. Nature, 2021, 589(7840): 131-136.
[17]
Liu X, Yu L, Hassan W, et al. The Duality of Kupffer Cell Responses in Liver Metabolic States [J]. Current Molecular Medicine, 2016, 16(9): 809-819.
[18]
Wan MJ, Han JW,, Ding Lili, et al. Novel Immune Subsets and Related Cytokines: Emerging Players in the Progression of Liver Fibrosis [J]. Frontiers in Medicine, 2021, 8: 604894.
[19]
Koyama Y, and Brenner DA. Liver inflammation and fibrosis [J]. Journal of Clinical Investigation, 2017, 127(1): 55-64.
[20]
Lim S, Kim JW, Targher G. Links between metabolic syndrome and metabolic dysfunction-associated fatty liver disease [J]. Trends in Endocrinology and Metabolism, 2021, 32(7): 500-514.
[21]
Ray I, Mahata SK, De RK. Obesity: An Immunometabolic Perspective [J]. Frontiers in Endocrinology, 2016, 7: 157.
[22]
Fink LN, Oberbach A, Costford SR, et al. Expression of anti-inflammatory macrophage genes within skeletal muscle correlates with insulin sensitivity in human obesity and type 2 diabetes [J]. Diabetologia, 2013, 56(7): 1623-1628.
[23]
Khan, IM, Perrard XY, Brunner G, et al. Intermuscular and perimuscular fat expansion in obesity correlates with skeletal muscle T cell and macrophage infiltration and insulin resistance [J]. International Journal of Obesity, 2015, 39(11): 1607-1618.
[24]
Citro A, Campo F, Dugnani E, et al. Innate Immunity Mediated Inflammation and Beta Cell Function: Neighbors or Enemies [J]. Frontiers in Endocrinology, 2020, 11: 606332.
[25]
Cosentino C, Regazzi R. Crosstalk between Macrophages and Pancreatic β-Cells in Islet Development, Homeostasis and Disease [J]. International Journal of Molecular Sciences, 2021, 22(4): 1765.
[26]
Böni-Schnetzler M, Meier DT. Islet inflammation in type 2 diabetes [J]. Seminars in Immunopathology, 2019, 41(4): 501-513.
[27]
Winer, DA, Luck H, Tsai S, et al. The Intestinal Immune System in Obesity and Insulin Resistance [J]. Cell Metabolism, 2016, 23(3): 413-426.
[28]
Ramírez-Pérez O, Cruz-Ramón V, Chinchilla-López P, et al. The Role of the Gut Microbiota in Bile Acid Metabolism [J]. Annals of Hepatology, 2017, 16 Suppl 1: S21-S26.
[29]
Torres-Fuentes C, Schellekens H, Dinan TG, et al. The microbiota-gut-brain axis in obesity [J]. The Lancet Gastroenterology & Hepatology, 2017, 2(10): 747-756.
[30]
Cox, AJ, West NP, Cripps AW. Obesity, inflammation, and the gut microbiota [J]. Lancet Diabetes & Endocrinology, 2015, 3(3): 207-215.
[31]
Moffa S, Mezza T, Cefalo CMA, et al. The Interplay between Immune System and Microbiota in Diabetes[J]. Mediators of Inflammation, 2019, 2019: 9367404.
[32]
Yuan M, Konstantopoulos N, Lee J, et al. Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta [J]. Science, 2001, 293(5535): 1673-1677.
[33]
Hawley, SA, Fullerton MD, Ross FA, et al. The ancient drug salicylate directly activates AMP-activated protein kinase [J]. Science, 2012, 336(6083): 918-922.
[34]
Ghanbari M, Momen Maragheh S, Aghazadeh A, et al. Interleukin-1 in obesity-related low-grade inflammation: From molecular mechanisms to therapeutic strategies [J]. International Immunopharmacology, 2021, 96: 107765.
[35]
Rissanen A, Howard CP, Botha J, et al. Effect of anti-IL-1β antibody (canakinumab) on insulin secretion rates in impaired glucose tolerance or type 2 diabetes: results of a randomized, placebo-controlled trial [J]. Diabetes Obesity & Metabolism, 2012, 14(12): 1088-1096.
[36]
Nanjan MJ, Mohammed M, Prashantha Kumar BR, et al. Thiazolidinediones as antidiabetic agents: A critical review [J]. Bioorganic Chemistry, 2018, 77: 548-567.
[37]
Yu SY, Cheng Y, Zhang LX, et al. Treatment with adipose tissue-derived mesenchymal stem cells exerts anti-diabetic effects, improves long-term complications, and attenuates inflammation in type 2 diabetic rats [J]. Stem Cell Research & Therapy, 2019, 10(1): 333.
[38]
Moon KC, Suh HS, Kim KB, et al. Potential of Allogeneic Adipose-Derived Stem Cell-Hydrogel Complex for Treating Diabetic Foot Ulcers [J]. Diabetes, 2019, 68(4): 837-846.
[39]
Akbari M, Hassan-Zadeh V. The inflammatory effect of epigenetic factors and modifications in type 2 diabetes [J]. Inflammopharmacology, 2020, 28(2): 345-362.
[40]
Zhao YS, Chen B, Shen J, et al. The Beneficial Effects of Quercetin, Curcumin, and Resveratrol in Obesity [J]. Oxidative Medicine and Cellular Longevity, 2017, 2017: 1459497.
[41]
Das B, Das M, Kalita A, et al. The role of Wnt pathway in obesity induced inflammation and diabetes: a review [J]. Journal of Diabetes & Metabolic Disorders, 2021, 20(2): 1871-1882.
[1] 何金梅, 尹立雪, 谭静, 张文军, 王锐, 任梅, 廖明娇. 超声心肌做功技术对2型糖尿病患者潜在左心室心肌收缩功能损伤的评价[J]. 中华医学超声杂志(电子版), 2023, 20(10): 1029-1035.
[2] 李永浩, 高雪菲, 郭田田, 张进, 张彩针, 刘静. 肥胖合并甲状腺癌相关机制的研究进展[J]. 中华普通外科学文献(电子版), 2023, 17(04): 311-315.
[3] 纪凯伦, 郝少龙, 孙海涛, 韩威. 减重术后胆囊结石形成机制的新进展[J]. 中华普外科手术学杂志(电子版), 2024, 18(01): 100-103.
[4] 陈大敏, 曹晓刚, 曹能琦. 肥胖对胃癌患者手术治疗效果的影响研究[J]. 中华普外科手术学杂志(电子版), 2023, 17(06): 651-653.
[5] 聂锋, 李婉珍. 不打针不吃药不输液徒手治疗糖尿病一例报道[J]. 中华普外科手术学杂志(电子版), 2023, 17(03): 354-354.
[6] 高文星, 刘浩, 赵稳, 李丁昌, 陈鹏, 金露佳, 刘先强, 董光龙. 减重手术后慢性腹痛的原因与对策[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 149-154.
[7] 汪赓, 夏泽锋, 陶凯雄. 代谢手术在非肥胖型2型糖尿病中的治疗效果及研究进展[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 155-160.
[8] 马俊蓉, 叶艳彬. 减重手术后的营养管理与复胖:现状与思考[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 165-172.
[9] 范晓轩, 王娜, 朱丽花, 王亮. 肥胖相关肿瘤研究进展[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 173-178.
[10] 李锦亮, 曾茂娟, 钟金宝, 何伟强, 林文新. 司美格鲁肽对肥胖2型糖尿病患者皮肤微循环功能的影响[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 192-196.
[11] 刘玉苓, 王婷婷, 吴高峰, 俞淑静. 健康体检人群内脏脂肪面积与新型炎症标志物的相关性研究[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 197-202.
[12] 刘澳, 周菁, 孙永兵, 和俊雅, 林新贝, 乔琦, 李中林, 张建成, 武肖玲, 邹智, 胡扬喜, 肖新广, 吕雪, 李昊, 李永丽. 减重代谢手术后神经影像改变与认知功能评估的研究进展[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 203-208.
[13] 秦梧耀, 高文惠, 崔浩, 尚吉文. 醛固酮与脂肪关系的研究进展[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 209-214.
[14] 陈笑梅, 陈文辉, 赵宛鄂, 郭婕, 苏超, 付志菊, 杨华, 董志勇, 王存川. 可吞咽自吸收新型胃内球囊治疗轻度肥胖症:一例病例报告[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 215-217.
[15] 由伟, 魏卓奇, 陈文辉, 董志勇, 杨华, 王存川. 腹腔镜细长胃囊Roux-en-Y胃旁路手术治疗重度肥胖症一例报道[J]. 中华肥胖与代谢病电子杂志, 2023, 09(03): 218-223.
阅读次数
全文


摘要