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DISCUSSION ON THE RELATIONSHIP BETWEEN METABOLIC SYNDROME AND OSTEOARTHRITIS

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Volume 2, Issue 1, Pp 8-13, 2024

DOI: 10.61784/wjbs240142

Author(s)

Collins Thomas

Affiliation(s)

Department of Bioengineering, Rice University, Houston, TX, USA.

Corresponding Author

Collins Thomas

ABSTRACT

Osteoarthritis (OA) is a multifactorial degenerative joint disease, mainly involving changes in articular cartilage, subchondral bone, ligaments, joint capsule, synovium and periarticular structures. Its pathogenesis remains unclear. As my country's population ages, the incidence of OA is gradually increasing. At the same time, most elderly patients are accompanied by basic metabolic diseases such as hypertension and diabetes. Metabolic osteoarthritis has now been identified as a new subtype of OA. In addition to surgical treatment, palliative treatment is the first choice, but its effect is limited. Therefore, metabolic osteoarthritis imposes a heavy burden on society and individuals, especially elderly patients. This article mainly introduces the current research status of the relationship between metabolic syndrome and osteoarthritis, and provides reference for the exploration of related targeted therapies.

KEYWORDS

Osteoarthritis; Metabolic syndrome; Adipocytokines; Macrophages; Intestinal flora

CITE THIS PAPER

Collins Thomas. Discussion on the relationship between metabolic syndrome and osteoarthritis. World Journal of Biomedical Sciences. 2024, 2(1): 8-13. DOI: 10.61784/wjbs240142.

REFERENCES

[1] Hunter DJ, Schofield D, Callander E. The individual and socioeconomic impact of osteoarthritis. Nat Rev Rheumatol, 2014, 10(7):437-441. DOI: 10.1038/nrrheum.2014.44.

[2] Pereira D, Peleteiro B, Araújo J. The effect of osteoarthritis definition on prevalence and incidence estimates: a systematic review. Osteoarthritis Cartilage, 2011, 19(11):1270-1285. DOI: 10.1016/j.joca.2011.08.009.

[3] Wallace IJ, Worthington S, Felson DT. Knee osteoarthritis has doubled in prevalence since the mid-20th century. Proc Natl Acad Sci U SA, 2017, 114(35):9332-9336. DOI: 10.1073/pnas.1703856114.

[4] Alberti KG, Eckel RH, Grundy SM. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation, 2009, 120(16):1640-1655. DOI: 10.1161/CIRCULATIONAHA.109.192644.

[5] Bortoluzzi A, Furini F, Scirè CA. Osteoarthritis and its management - Epidemiology, nutritional aspects and environmental factors. Autoimmun Rev, 2018, 17(11): 1097-1104. DOI: 10.1016/j.autrev.2018.06.002.

[6] Michalek RD, Rathmell JC. The metabolic life and times of a T-cell. Immunol Rev, 2010, 236:190-202. DOI: 10.1111/j.1600-065X.2010.00911.x.

[7] Mobasheri A, Rayman MP, Gualillo O. The role of metabolism in the pathogenesis of osteoarthritis. Nat Rev Rheumatol, 2017, 13(5):302-311. DOI: 10.1038/nrrheum. 2017.50.

[8] Kolasinski SL, Neogi T, Hochberg MC. 2019 American College of Rheumatology/Arthritis Foundation Guideline for the management of osteoarthritis of the hand, hip, and knee. Arthritis Care Res (Hoboken), 2020, 72(2):149-162. DOI:10.1002/acr.24131.

[9] Berenbaum F, Eymard F, Houard X. Osteoarthritis, inflammation and obesity. Curr Opin Rheumatol, 2013, 25(1):114-118. DOI: 10.1097/BOR.0b013e32835a9414.

[10] Engstr?m G, Gerhardsson de Verdier M, Rollof J. C-reactive protein, metabolic syndrome and incidence of severe hip and knee osteoarthritis. A population-based cohort study. Osteoarthritis Cartilage, 2009, 17(2):168-713. DOI: 10.1016/j.joca.2008.07.003.

[11] Vieira-Potter VJ. Inflammation and macrophage modulation in adipose tissues. Cell Microbiol, 2014, 16(10):1484-1492. DOI: 10.1111/cmi.12336.

[12] Francisco V, Ruiz-Fernández C, Pino J. Adipokines: linking metabolic syndrome, the immune system, and arthritic diseases. Biochem Pharmacol, 2019, 165:196-206. DOI: 10.1016/j.bcp.2019.03.030.

[13] Xie C, Chen Q. Adipokines: new therapeutic target for osteoarthritis? Curr Rheumatol Rep, 2019, 21(12):71. DOI: 10.1007/s11926-019-0868-z.

[14] Sun Y, Xun K, Wang C. Adiponectin, an unlocking adipocytokine. Cardiovasc Ther, 2009, 27(1):59-75. DOI: 10.1111/j.1755-5922.2008.00069.x.

[15] Liu M, Liu F. Regulation of adiponectin multimerization, signaling and function. Best Pract Res Clin Endocrinol Metab, 2014, 28(1):25-31. DOI: 10.1016/j.beem.2013.06.003.

[16] Kim ES, Im JA, Kim KC. Improved insulin sensitivity and adiponectin level after exercise training in obese korean youth. Obesity (Silver Spring), 2007, 15(12):3023-3030. DOI: 10.1038/oby.2007.360.

[17] Hu J, Cui W, Ding W. Globular adiponectin attenuated H2O2-induced apoptosis in rat chondrocytes by inducing autophagy through the AMPK/mTOR pathway. Cell Physiol Biochem, 2017, 43(1):367-382. DOI: 10.1159/000480416.

[18] Landgraeber S, Putz S, Schlattjan M. Adiponectin attenuates osteolysis in aseptic loosening of total hip replacements. Acta Biomater, 2014, 10(1):384-393. DOI: 10.1016/j.actbio.2013.08.031.

[19] Conde J, Gomez R, Bianco G. Expanding the adipokine network in cartilage: identification and regulation of novel factors in human and murine chondrocytes. Ann Rheum Dis, 2011, 70(3):551-559. DOI: 10.1136/ard.2010.132399.

[20] Li WC, Hsiao KY, Chen IC. Serum leptin is associated with cardiometabolic risk and predicts metabolic syndrome in Taiwanese adults. Cardiovasc Diabetol, 2011, 10:36. DOI: 10.1186/1475-2840-10-36.

[21] Panchal SK, Poudyal H, Iyer A. High-carbohydrate, high-fat diet-induced metabolic syndrome and cardiovascular remodeling in rats. J Cardiovasc Pharmacol, 2011, 57(5): 611-624. DOI: 10.1097/FJC.0b013e31821b1379.

[22] Dumond H, Presle N, Terlain B. Evidence for a key role of leptin in osteoarthritis. Arthritis Rheum, 2003, 48(11):3118-3129. DOI: 10.1002/art.11303.

[23] Gómez R, Scotece M, Conde J. Adiponectin and leptin increase IL-8 production in human chondrocytes. Ann Rheum Dis, 2011, 70(11):2052-2054. DOI: 10.1136/ard.2010.145672.

[24] Abella V, Scotece M, Conde J. The potential of lipocalin-2/NGAL as biomarker for inflammatory and metabolic diseases. Biomarkers, 2015, 20(8):565-571. DOI: 10.3109/1354750X.2015.1123354.

[25] Jang Y, Lee JH, Wang Y. Emerging clinical and experimental evidence for the role of lipocalin-2 in metabolic syndrome. Clin Exp Pharmacol Physiol, 2012, 39(2): 194-199. DOI: 10.1111/j.1440-1681.2011.05557.x.

[26] Dickson BM, Roelofs AJ, Rochford JJ. The burden of metabolic syndrome on osteoarthritic joints. Arthritis Res Ther, 2019, 21(1):289. DOI: 10.1186/s13075-019-2081-x.

[27] Blom AB, van Lent PL, Holthuysen AE. Synovial lining macrophages mediate osteophyte formation during experimental osteoarthritis. Osteoarthritis Cartilage, 2004, 12(8):627-635. DOI: 10.1016/j.joca.2004.03.003.

[28] Kraus VB, McDaniel G, Huebner JL. Direct in vivo evidence of activated macrophages in human osteoarthritis. Osteoarthritis Cartilage, 2016, 24(9):1613-1621. DOI: 10.1016/j.joca.2016.04.010.

[29] Bondeson J, Blom AB, Wainwright S. The role of synovial macrophages and macrophage-produced mediators in driving inflammatory and destructive responses in osteoarthritis. Arthritis Rheum, 2010, 62(3):647-657. DOI: 10.1002/art.27290.

[30] Raghu H, Lepus CM, Wang Q. CCL2/CCR2, but not CCL5/CCR5, mediates monocyte recruitment, inflammation and cartilage destruction in osteoarthritis. Ann Rheum Dis, 2017, 76(5):914-922. DOI: 10.1136/annrheumdis- 2016-210426.

[31] Fan Q, Liu Z, Shen C. Microarray study of gene expression profile to identify new candidate genes involved in the molecular mechanism of leptin-induced knee joint osteoarthritis in rat. Hereditas, 2017, 155:4. DOI: 10.1186/s41065-017-0039-z.

[32] Kierdorf K, Fritz G. RAGE regulation and signaling in inflammation and beyond. J Leukoc Biol, 2013, 94(1):55-68. DOI: 10.1189/jlb.1012519.

[33] Rogero MM, Calder PC. Obesity, inflammation, toll-like receptor 4 and fatty acids. Nutrients, 2018, 10(4):432. DOI: 10.3390/nu10040432.

[34] Jandhyala SM, Talukdar R, Subramanyam C. Role of the normal gut microbiota. World J Gastroenterol, 2015, 21(29):8787-8803. DOI: 10.3748/wjg.v21.i29.8787.

[35] Guss JD, Ziemian SN, Luna M. The effects of metabolic syndrome, obesity, and the gut microbiome on load-induced osteoarthritis. Osteoarthritis Cartilage, 2019, 27(1):129-139. DOI: 10.1016/j.joca.2018.07.020.

[36] Boer CG, Radjabzadeh D, Medina-Gomez C. Intestinal microbiome composition and its relation to joint pain and inflammation. Nat Commun, 2019, 10(1):4881. DOI: 10.1038/s41467-019-12873-4.

[37] Cani PD. Crosstalk between the gut microbiota and the endocannabinoid system: impact on the gut barrier function and the adipose tissue. Clin Microbiol Infect, 2012, 18(Suppl 4): 50-53. DOI: 10.1111/j.1469-0691.2012.03866.x.

[38] Wang J, Tang H, Zhang C. Modulation of gut microbiota during probiotic-mediated attenuation of metabolic syndrome in high fat diet-fed mice. ISME J, 2015, 9(1):1-15. DOI: 10.1038/ismej.2014.99.

[39] Yoo JY, Kim SS. Probiotics and prebiotics: present status and future perspectives on metabolic disorders. Nutrients, 2016, 8(3):173. DOI: 10.3390/nu8030173.

[40] Schott EM, Farnsworth CW, Grier A. Targeting the gut microbiome to treat the osteoarthritis of obesity. JCI Insight, 2018, 3(8):e95997. DOI: 10.1172/jci.insight.95997.

[41] Steves CJ, Bird S, Williams FM. The microbiome and musculoskeletal conditions of aging: a review of evidence for impact and potential therapeutics. J Bone Miner Res, 2016, 31(2):261-269. DOI: 10.1002/jbmr.2765.

[42] Miura K, Ishioka M, Iijima K. The roles of the gut microbiota and toll-like receptors in obesity and nonalcoholic fatty liver disease. J Obes Metab Syndr, 2017, 26(2):86-96. DOI: 10.7570/jomes.2017.26.2.86.

[43] Ulici V, Kelley KL, Azcarate-Peril MA. Osteoarthritis induced by destabilization of the medial meniscus is reduced in germ-free mice. Osteoarthritis Cartilage, 2018, 26(8): 1098-1109. DOI: 10.1016/j.joca.2018.05.016.

[44] Cheng J, Xue F, Zhang M. TRIM31 Deficiency is associated with impaired glucose metabolism and disrupted gut microbiota in mice. Front Physiol, 2018, 9:24. DOI: 10.3389/fphys.2018.00024.

[45] Huang Z, Chen J, Li B. Faecal microbiota transplantation from metabolically compromised human donors accelerates osteoarthritis in mice. Ann Rheum Dis, 2020, 79(5):646-656. DOI: 10.1136/annrheumdis-2019-216471.

[46] Niu J, Clancy M, Aliabadi P. Metabolic syndrome, its components, and knee osteoarthritis: the framingham osteoarthritis study. Arthritis Rheumatol, 2017, 69(6): 1194-1203. DOI: 10.1002/art.40087.

[47] Xie Y, Zhou W, Zhong Z. Metabolic syndrome, hypertension, and hyperglycemia were positively associated with knee osteoarthritis, while dyslipidemia showed no association with knee osteoarthritis. Clin Rheumatol, 2021, 40(2):711-724. DOI: 10.1007/s10067-020-05216-y.

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