open access

Vol 71, No 2 (2020)
Original Paper
Published online: 2020-03-04
Submitted: 2019-12-01
Accepted: 2020-01-09
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Peripheral levels of selected adipokines in patients with newly diagnosed multiple sclerosis

Agnieszka Baranowska-Bik, Dorota Uchman, Anna Litwiniuk, Małgorzata Kalisz, Lidia Martyńska, Bogusława Baranowska, Wojciech Bik, Jan Kochanowski
DOI: 10.5603/EP.a2020.0008
·
Pubmed: 32154570
·
Endokrynologia Polska 2020;71(2):109-115.

open access

Vol 71, No 2 (2020)
Original Paper
Published online: 2020-03-04
Submitted: 2019-12-01
Accepted: 2020-01-09

Abstract

Introduction: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system. The exact aetiology is unknown. However, genetic and environmental factors are suggested to be involved in the pathogenesis of MS. Improper diet, resulting in obesity and metabolic syndrome, can contribute to this disease. Adipokines, secreted by adipose tissue, link the metabolism and immune system.

Material and methods: We aimed to assess plasma levels of selected adipokines in newly diagnosed, treatment-naïve individuals with multiple sclerosis. Our group comprised 58 individuals (31 MS patients and 27 controls, matched for age and BMI) without diabetes, hypertension, or dyslipidaemia. Circulating adiponectin and all adiponectin fractions, visfatin, and omentin concentrations were measured. Metabolic parameters were also assessed.

Results: In MS individuals we observed the following results: higher concentrations of visfatin, lower levels of omentin, and no differences in adiponectin array. There were also correlations between some adipokines and metabolic parameters. After adjustment to BMI, a significant decrease in total adiponectin, high-molecular weight (HMW) adiponectin and omentin, and an increase in medium-molecular-weight (MMW) adiponectin were observed in the group of MS patients when compared to those of the controls.

Conclusions: Our results indicate that adiponectin with its fractions, visfatin, and omentin cannot be considered as causative factors in the early phase of multiple sclerosis. However, the potential role of adipokines in MS is possible because they might be involved in the pathogenesis of MS, regarded as an autoimmune disorder. 

Abstract

Introduction: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system. The exact aetiology is unknown. However, genetic and environmental factors are suggested to be involved in the pathogenesis of MS. Improper diet, resulting in obesity and metabolic syndrome, can contribute to this disease. Adipokines, secreted by adipose tissue, link the metabolism and immune system.

Material and methods: We aimed to assess plasma levels of selected adipokines in newly diagnosed, treatment-naïve individuals with multiple sclerosis. Our group comprised 58 individuals (31 MS patients and 27 controls, matched for age and BMI) without diabetes, hypertension, or dyslipidaemia. Circulating adiponectin and all adiponectin fractions, visfatin, and omentin concentrations were measured. Metabolic parameters were also assessed.

Results: In MS individuals we observed the following results: higher concentrations of visfatin, lower levels of omentin, and no differences in adiponectin array. There were also correlations between some adipokines and metabolic parameters. After adjustment to BMI, a significant decrease in total adiponectin, high-molecular weight (HMW) adiponectin and omentin, and an increase in medium-molecular-weight (MMW) adiponectin were observed in the group of MS patients when compared to those of the controls.

Conclusions: Our results indicate that adiponectin with its fractions, visfatin, and omentin cannot be considered as causative factors in the early phase of multiple sclerosis. However, the potential role of adipokines in MS is possible because they might be involved in the pathogenesis of MS, regarded as an autoimmune disorder. 

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Keywords

adiponectin; adiponectin fractions; visfatin; omentin; multiple sclerosis

About this article
Title

Peripheral levels of selected adipokines in patients with newly diagnosed multiple sclerosis

Journal

Endokrynologia Polska

Issue

Vol 71, No 2 (2020)

Pages

109-115

Published online

2020-03-04

DOI

10.5603/EP.a2020.0008

Pubmed

32154570

Bibliographic record

Endokrynologia Polska 2020;71(2):109-115.

Keywords

adiponectin
adiponectin fractions
visfatin
omentin
multiple sclerosis

Authors

Agnieszka Baranowska-Bik
Dorota Uchman
Anna Litwiniuk
Małgorzata Kalisz
Lidia Martyńska
Bogusława Baranowska
Wojciech Bik
Jan Kochanowski

References (43)
  1. Dilokthornsakul P, Valuck RJ, Nair KV, et al. Multiple sclerosis prevalence in the United States commercially insured population. Neurology. 2016; 86(11): 1014–1021.
  2. Martin R, Sospedra M, Rosito M, et al. Current multiple sclerosis treatments have improved our understanding of MS autoimmune pathogenesis. Eur J Immunol. 2016; 46(9): 2078–2090.
  3. Guerrero-García Jd, Carrera-Quintanar L, López-Roa RI, et al. Multiple Sclerosis and Obesity: Possible Roles of Adipokines. Mediators Inflamm. 2016; 2016: 4036232.
  4. Thompson A, Baranzini S, Geurts J, et al. Multiple sclerosis. Lancet. 2018; 391(10130): 1622–1636.
  5. Gianfrancesco MA, Barcellos LF. Obesity and Multiple Sclerosis Susceptibility: A Review. J Neurol Neuromedicine. 2016; 1(7): 1–5.
  6. Versini M, Jeandel PY, Rosenthal E, et al. Obesity in autoimmune diseases: not a passive bystander. Autoimmun Rev. 2014; 13(9): 981–1000.
  7. Dyaczyński M, Scanes CG, Koziec H, et al. Endocrine implications of obesity and bariatric surgery. Endokrynol Pol. 2018; 69(5): 574–597.
  8. Bilir BE, Güldiken S, Tunçbilek N, et al. The effects of fat distribution and some adipokines on insulin resistance. Endokrynol Pol. 2016; 67(3): 277–282.
  9. Orlando A, Nava E, Giussani M, et al. Adiponectin and Cardiovascular Risk. From Pathophysiology to Clinic: Focus on Children and Adolescents. Int J Mol Sci. 2019; 20(13).
  10. Shehzad A, Iqbal W, Shehzad O, et al. Adiponectin: regulation of its production and its role in human diseases. Hormones (Athens). 2012; 11(1): 8–20.
  11. Liu M, Liu F. Regulation of adiponectin multimerization, signaling and function. Best Pract Res Clin Endocrinol Metab. 2014; 28(1): 25–31.
  12. Li P, Yang Li, Ma CL, et al. Low-molecular-weight adiponectin is more closely associated with disease activity of rheumatoid arthritis than other adiponectin multimeric forms. Clin Rheumatol. 2015; 34(6): 1025–1030.
  13. Achari AE, Jain SK. Adiponectin, a Therapeutic Target for Obesity, Diabetes, and Endothelial Dysfunction. Int J Mol Sci. 2017; 18(6).
  14. Ouchi N, Walsh K. A novel role for adiponectin in the regulation of inflammation. Arterioscler Thromb Vasc Biol. 2008; 28(7): 1219–1221.
  15. Yokota T, Oritani K, Takahashi I, et al. Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. Blood. 2000; 96(5): 1723–1732.
  16. Makki K, Froguel P, Wolowczuk I. Adipose tissue in obesity-related inflammation and insulin resistance: cells, cytokines, and chemokines. ISRN Inflamm. 2013; 2013: 139239.
  17. Neumeier M, Weigert J, Schäffler A, et al. Different effects of adiponectin isoforms in human monocytic cells. J Leukoc Biol. 2006; 79(4): 803–808.
  18. He Y, Lu L, Wei X, et al. The multimerization and secretion of adiponectin are regulated by TNF-alpha. Endocrine. 2016; 51(3): 456–468.
  19. Mayi TH, Duhem C, Copin C, et al. Visfatin is induced by peroxisome proliferator-activated receptor gamma in human macrophages. FEBS J. 2010; 277(16): 3308–3320.
  20. Xiao Ke, Zou WH, Yang Z, et al. The role of visfatin on the regulation of inflammation and apoptosis in the spleen of LPS-treated rats. Cell Tissue Res. 2015; 359(2): 605–618.
  21. Kumari B, Yadav UCS. Adipokine Visfatin's Role in Pathogenesis of Diabesity and Related Metabolic Derangements. Curr Mol Med. 2018; 18(2): 116–125.
  22. Stofkova A. Resistin and visfatin: regulators of insulin sensitivity, inflammation and immunity. Endocr Regul. 2010; 44(1): 25–36.
  23. Yang RZ, Lee MJ, Hu H, et al. Identification of omentin as a novel depot-specific adipokine in human adipose tissue: possible role in modulating insulin action. Am J Physiol Endocrinol Metab. 2006; 290(6): E1253–E1261.
  24. Escoté X, Gómez-Zorita S, López-Yoldi M, et al. Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development. Int J Mol Sci. 2017; 18(8).
  25. Watanabe T, Watanabe-Kominato K, Takahashi Y, et al. Adipose Tissue-Derived Omentin-1 Function and Regulation. Compr Physiol. 2017; 7(3): 765–781.
  26. Baranowska-Bik A, Kalisz M, Martyńska L, et al. Plasma adiponectin array in women with Alzheimer's disease. Endokrynol Pol. 2018; 69(5): 550–559.
  27. Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol. 2011; 69(2): 292–302.
  28. Hietaharju A, Kuusisto H, Nieminen R, et al. Elevated cerebrospinal fluid adiponectin and adipsin levels in patients with multiple sclerosis: a Finnish co-twin study. Eur J Neurol. 2010; 17(2): 332–334.
  29. Penesova A, Vlcek M, Imrich R, et al. Hyperinsulinemia in newly diagnosed patients with multiple sclerosis. Metab Brain Dis. 2015; 30(4): 895–901.
  30. Signoriello E, Lus G, Polito R, et al. Adiponectin profile at baseline is correlated to progression and severity of multiple sclerosis. Eur J Neurol. 2019; 26(2): 348–355.
  31. Palavra F, Marado D, Mascarenhas-Melo F, et al. New markers of early cardiovascular risk in multiple sclerosis patients: oxidized-LDL correlates with clinical staging. Dis Markers. 2013; 34(5): 341–348.
  32. Düzel B, Tamam Y, Çoban A, et al. Adipokines in Multiple Sclerosis Patients with and without Optic Neuritis as the First Clinical Presentation. Immunol Invest. 2019; 48(2): 190–197.
  33. Kraszula L, Jasińska A, Eusebio MO, et al. Evaluation of the relationship between leptin, resistin, adiponectin and natural regulatory T cells in relapsing-remitting multiple sclerosis. Neurol Neurochir Pol. 2012; 46(1): 22–28.
  34. Musabak U, Demirkaya S, Genç G, et al. Serum adiponectin, TNF-α, IL-12p70, and IL-13 levels in multiple sclerosis and the effects of different therapy regimens. Neuroimmunomodulation. 2011; 18(1): 57–66.
  35. Yousefian M, Nemati R, Daryabor G, et al. Gender-Specific Association of Leptin and Adiponectin Genes With Multiple Sclerosis. Am J Med Sci. 2018; 356(2): 159–167.
  36. Çoban A, Düzel B, Tüzün E, et al. Investigation of the prognostic value of adipokines in multiple sclerosis. Mult Scler Relat Disord. 2017; 15: 11–14.
  37. Kvistad SS, Myhr KM, Holmøy T, et al. Body mass index influence interferon-beta treatment response in multiple sclerosis. J Neuroimmunol. 2015; 288: 92–97.
  38. Devorak J, Mokry LE, Morris JA, et al. Large differences in adiponectin levels have no clear effect on multiple sclerosis risk: A Mendelian randomization study. Mult Scler. 2017; 23(11): 1461–1468.
  39. Piccio L, Cantoni C, Henderson JG, et al. Lack of adiponectin leads to increased lymphocyte activation and increased disease severity in a mouse model of multiple sclerosis. Eur J Immunol. 2013; 43(8): 2089–2100.
  40. Zhang K, Guo Y, Ge Z, et al. Adiponectin Suppresses T Helper 17 Cell Differentiation and Limits Autoimmune CNS Inflammation via the SIRT1/PPARγ/RORγt Pathway. Mol Neurobiol. 2017; 54(7): 4908–4920.
  41. Emamgholipour S, Eshaghi SM, Hossein-nezhad A, et al. Adipocytokine profile, cytokine levels and foxp3 expression in multiple sclerosis: a possible link to susceptibility and clinical course of disease. PLoS One. 2013; 8(10): e76555.
  42. Mirzaei K, Hossein-Nezhad A, Mokhtari F, et al. Visfatin/NAMPT/PBCEF and Cytokine Concentration in Multiple Sclerosis Patients Compared to Healthy Subjects. Eur J Inflamm. 2011; 9(1): 31–37.
  43. Assadi M, Salimipour H, Akbarzadeh S, et al. Correlation of circulating omentin-1 with bone mineral density in multiple sclerosis: the crosstalk between bone and adipose tissue. PLoS One. 2011; 6(9): e24240.

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