The value of the tumor necrosis factor-alpha and vaspin ratio in the development of insulin resistance


  • Zhuravlyova L. V. Kharkiv National Medical University, Kharkiv, Ukraine
  • Pylov D. I. Kharkiv National Medical University, Kharkiv, Ukraine



vaspin, tumor necrosis factor alpha, adipocytokines, insulin resistance


Diabetes mellitus type 2 is a chronic disease that results in metabolic disorders in the whole organism, primarily due to insulin resistance and relative insufficiency of insulin. The fatty tissue is no longer considered only as a passive depositary for the accumulation of energy and participation in the regulation of thermogenesis. In the last decades, it has been noted that this is an active endocrine organ that in addition to regulation of fat mass and participating in homeostasis, also releases a large number of bioactive mediators called adipokines. Adipokines are influenced by an autocrine or paracrine method on a variety of metabolic processes. Increased body weight is a factor in the development of different metabolic disorders. Excess fatty tissue can directly affect one of the main metabolic links — activity and insulin sensitivity. Increased body weight is a factor in the development of a carbohydrate metabolism disorder. Vaspin is an adipocytokine, a representative of widely spread serpins (serine protease inhibitors). The elevated serum protease inhibitor profile was noted in overweight and insulin-resistant mice. It is suggested that vaspin is an insulin sensitizer with anti-inflammatory action and can take part as a compensatory mechanism in response to reduced insulin sensitivity. Therefore, the activation of vaspin may decrease insulin resistance. Evaluation of protease which can be inhibited by vaspin may increase the development of new approaches of compensation based on etiology of impaired metabolic and glucose tolerance. The tumor necrosis factor-α (TNF-α) is a cytokine that is involved in systemic inflammation. The elevated levels of TNF-α are considered as one of the causative factors in insulin resistance, which is associated with obesity in the pathogenesis of DM-2. This review article provides an analysis of mostly foreign scientific articles about the importance of adipokines, particularly TNF-α and vaspin, in the development of insulin resistance and the possibility of further consideration of these markers as an indicator of the severity of the impaired carbohydrate metabolism.


Zheng Y, Ley SH, Hu FB. Nat Rev Endocrinol 2018; 14(2): 88-98.

Unnikrishnan R, Pradeepa R, Joshi SR, Mohan V. Diabetes 2017; 66(6): 1432-1442.

Unifikovanyj klinichnyj protokol pervynnoi’, ekstrenoi’, vtorynnoi’ (specializovanoi’) ta tretynnoi’ (vysokospecializovanoi’) medychnoi’ dopomogy. Cukrovyj diabet u molodyh ljudej ta doroslyh, 2014;1021, available at:

Travers ME, McCarthy MI. Hum Genet 2011; 130(1): 41- 58.

Elochukwu AC, Opara UC, Chinyere NA, et al. Trop J Med Res 2 017; 2 0: 4 5-52.

Smitka K, Maresova D. Prague Med Rep 2015; 116(2): 87-111.

Akash MS, Rehman K, Chen S. J Cell Biochem 2013; 114(3): 525-531.

Zozulinska D, Wierusz-Wysocka B. Diabetes Res Clin Pract 2006; 74: S12-S16.

Mirodzhov GK, Avezov SA, Amirkulova MM, et al. Doklady Akademii nauk respubliki Tadzhikistan 2013; 56(8): 562-566.

Akash MSH, Rehman K, Sun H, Chen S. Eur J Pharmacol 2013; 701: 87-95.

Memon AA, Sundquist J, Wang X, et al. BMJ Open 2013; 3: e003473.

Feve B, Bastard JP. Nat Rev Endocrinol 2 009; 5 (6): 305-311.

Aggarwal BB, Gupta SC, Kim JH. Blood 2012; 119(3): 651-665.

Ehlers S. Ann Rheum Dis 2003; 62: ii37-ii42.

Fischer R, Maier O. Oxid Med Cell Longev 2015; 2015: 610813.

Imai Y, Dobrian AD, Weaver JR, et al. Diabetes Obes Metab 2013; 15(3): 117-129.

Richter EA. Physiol Rev 2013;93(3): 993-1017.

Fasshauer M, Paschke R. Diabetologia 2003; 46: 1594-1603.

Carter-Kent C, Zein NN, Feldstein AE. Am J Gastroenterol 2008; 103: 1036-1042.

Dong Y, Dekens DW, De Deyn PP, et al. Antibodies 2015; 4: 369-408.

Ruan H, Lodish HF. Cytokine Growth Factor Rev 2003; 14: 447-455.

Cawthorn WP, Sethi JK. FEBS Lett 2008; 582: 117-131.

Liu C, Feng X, Li Q, et al. Cytokine 2016; 86: 100-109.

Hamada D, Maynard R, Schott E, et al. Arthritis Rheum 2016; 68: 1392-1402.

Miyazaki Y, Pipek R, Mandarino L, DeFronzo RA. Int J Obes 2003; 27: 88-94.

Hotamisligil GS. Nature Vol 2006; 444: 860-867.

da Rocha AF, Liboni TF, Kurauti MA, et al. Pharmacol Rep 2014;66: 380-385.

Shoelson SE, Lee J, Goldfine AB. J Clin Invest 2006; 116: 1793-1801.

Steinberg GR. Cell Cycle 2007; 6: 888-894.

Hirosumi J, Tuncman G, Chang L, et al. Nature 2002; 420: 333-336.

Hida K, Wada J, Eguchi J, et al. Proc Natl Acad Sci USA 2005; 102: 10610-

Heiker JT, Klцting N, Kovacs P, et al. Cell Mol Life Sci 2013; 70: 2569-2583.

Luo X, Li K, Zhang C, et al. Int J Obes (Lond) 2016; 40: 947-954.

Castro CA, da Silva KA, Buffo MM, et al. Int J Exp Pathol 2017; 98(1): 26-33.

Saad MJA, Santos A, Prada PO. Physiology 2016; 31: 283-293.

Qi D, Wang D, Zhang C, et al. Int J Mol Med 2017; 40: 1803-1817.

Рhalitakul S, Okada M, Hara Y, Yamawaki H. Pharmacol Res 2011;64: 493-500.

Liu S, Dong Y, Wang T, et al. Diabetes Res Clin Pract 2014; 103: 482-488.

Goktas Z, Owens S, Boylan M, et al. Mediators Inflamm 2013; 2013: 1-9.

Feng R, Li Y, Wang C, et al. Diabetes Res Clin Pract 2014; 106(1): 88-94.

Jian W, Peng W, Xiao S, et al. PLoS One 2014; 9(4): e94763.

Dai R, Dong Z, Qian Y, Han Y. J Diabetes 2016; 8: 445-447.

Salek-Maghsoudi A, Hassani S, Momtaz S, et al. Toxicology 2019; 411: 1-14.




How to Cite

Zhuravlyova, L. V., & Pylov, D. I. (2019). The value of the tumor necrosis factor-alpha and vaspin ratio in the development of insulin resistance. Problems of Endocrine Pathology, 69(3), 113-120.