Serum visfatin in type 2 diabetes mellitus

Samiha A. Abd Rabo1, Nagwa Abd EL-Ghaffar1, Somayh S. Eissa1, Abeer A. Ali1, Sahar Mohamed Ismail1, Reham S. Gad2
1Department of Internal Medicine, Faculty of Medicine for Girls, Al-Azhar University, 131 Saker Quriesh, New Maadi, Cairo, Egypt
2Department of Internal Medicine, Matareya Teaching Hospital, Cairo, Egypt

Tóm tắt

Abstract Introduction Obesity is commonly associated with insulin resistance and hyperinsulinemia and is the most important risk factor for type 2 diabetes. Visfatin is an adipokine that exerts insulin-mimetic effects that stimulate muscle and adipocyte glucose transport and inhibit hepatocyte glucose production. Purpose The aim of this study was to assess levels of visfatin and its relationship to obesity and insulin resistance in type 2 diabetes mellitus. Patients and methods This study included 40 patients with type 2 diabetes as the patient group: 20 of them were obese (BMI ≥ 30) and 20 were not (BMI < 25). Forty apparently healthy individuals matched for age and sex were included as the control group: 20 of them were obese (BMI ≥ 30) and the other 20 were not (BMI < 25). All patients and controls underwent history taking, physical examination including determination of BMI, and the following laboratory investigations: determination of levels of fasting blood glucose, 2 h postprandial blood glucose, serum cholesterol, triglycerides, fasting insulin, and fasting visfatin; kidney and liver function tests and calculation of homeostasis model of assessment-insulin resistance (HOMA-IR) were also performed. Neither the patients nor controls suffered from any chronic disease other than diabetes. Results The results of this study revealed a highly significant increase in the fasting serum insulin level, HOMA-IR, and fasting serum visfatin level among diabetic patients (26.10 ± 6.04μIU/ml, 12.18 ± 5.24, 36.70 ± 6.86 ng/ml, respectively) when compared with controls (12.10 ± 3.45μIU/ml, 2.42 ± 0.79, 13.63 ± 3.98 ng/ml, respectively; P < 0.01). Fasting insulin levels, HOMA-IR, and visfatin levels were significantly higher in obese diabetic patients (31.13 ± 4.34μIU/ml, 14.71 ± 6.22, 42.36 ± 4.11 ng/ml, respectively) than in obese controls (14.31±3.11mIU/ml, 2.89±0.77, 16.72 ± 3.16 ng/ml, respectively; P < 0.01). Visfatin levels were higher in nonobese diabetic patients than in nonobese controls. Moreover, visfatin levels were higher in obese diabetic patients (31.04 ± 3.49 ng/ml) than in nonobese diabetic patients (10.54 ± 1.53 ng/ml; P < 0.01). The present study revealed a highly significant positive correlation between levels of visfatin and fasting insulin in both obese and nonobese diabetic patients. Although there was a significant positive correlation between visfatin levels and HOMA-IR, there was no significant correlation between visfatin levels and BMI in obese diabetic patients. Conclusion Visfatin levels are increased in patients with type 2 diabetes regardless the degree of adiposity.

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Tài liệu tham khảo

Arya M, Sharma MD. The obese patient with diabetes mellitus: from research targets to treatment options. Am J Med 2006; 119 (5A): 17S–23S.

Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004; 89:2548–2556.

Chen MP, Chung FM, Chang DM, Tsai JC, Huang HF, Shin SJ, Lee YJ. Elevated plasma level of visfatin/pre-B cell colony-enhancing factor in patients with type 2 diabetes mellitus. J Clin Endocrinol Metab 2006; 91:295–299.

Dotsch J, Rascher W, Meibner U. Dose visceral fats produce insulin. Eur J Endocrinol 2005; 153:475–476.

Curat CA, Wegner V, Sengenes C, Miranville A, Tonus C, Busse R, Bouloumie A. Macrophages in human visceral adipose tissues: increased accumulation in obesity and a source of resistin and visfatin. Diabetologia 2006; 49:744–747.

Adghate E. Visfatin: structure, function and relation to diabetes mellitus and other dysfunctions. Curr Med Chem 2008; 15:1851–1862.

Ognjanovic S, Bao S, Yamamoto SY, Garibay-tupas J, Samal B, Brayant-Greenwood GD. Genomic organization of the gene coding for human pre B-cell colony enhancing factor and expression in human fetal membranes. J Mol Edocrinol 2001; 26:107–117.

Mauser W, Perwitz N, Meier B, Fasshauer M, Klein J. Direct adipotropic action of atorvastatin: differentiation state dependent induction of apoptosis, modulation of endocrine function, and inhibition of glucose uptake. Eur J Pharmacol 2007; 564:37–46.

Kim SR, Bae SK, Choi KS, Park SY, Jun HO, Lee JY, et al. Visfatin promotes angiogenesis by activation of extracellular signal-regulated kinase 1/2. Biochem Biophys Res Commun 2007; 357:150–156.

Fukuhara A, Matsuda M, Nishezawa M, Segawa K, Tanaka M, Kishimoto K, et al. Visfatin: a protein secreted by visceral fat that mimics the effect of insulin. Science 2005; 307:426–430.

Chang YH, Chang DM, Lin KC, Shin SJ, Lee YJ. Visfatin in overweight/ obesity, type 2 diabetes mellitus, insulin resistance, metabolic syndrome and cardiovascular diseases: a meta-analysis and systemic review. Diabetes Metab Res Rev 2011; 27:515–527.

Esteghamati A, Alamdari A, Zandieh A, Elahi S, Khalilzadeh O, Nakhjavani M, Meysamie A. Serum visfatin is associated with type 2 diabetes mellitus independent of insulin resistance and obesity. Diabetes Res Clin Pract 2011; 91:154–158.

Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care 2004; 27:1487–1495.

Garten A, Petzold S, Barnikol-Oettler A, Körner A, Thasler WE, Kratzsch J, et al. Nicotinamide phosphoribosyltransferase (NAMPT/PBEF/visfatin) is constitutively released from human hepatocytes. Biochem Biophys Res Commun 2010; 391:376–381.

Varma V, Yao A, Rasouli N, Angela M, Lee M, Starks T, et al. human serum visfatin expression: relationship to insulin sensitivity, intramyocellular lipids, and inflammation. J Clin Endocrinol Metab 2006; 92:666–672.

Zahorska-Makiewicz B, Olszanecka-Glinianowicz M, Janwaska J, Kocelak P, Semik-Grabarczyk E, Holecki M, et al. Serum concentration of visfatin in obese women. Metabolism 2007; 56:1131–1134.

Hammarstedt A, Pihlajamaki J, Sopasaki VR, Gogg S, Jansson PA, Laakso M. Visfatin is an adipokine, but it is not regulated by thiazolidinediones. J Clin Endocrinol Metab 2006; 91:1181–1184.

Sandeep S, Velmurugan K, Deepa R, Mohan V. Serum visfatin in relation to visceral fats, obesity, type 2 diabetes mellitus in Asian Indians. Metabolism 2007; 56:565–570.

Abdullah A, Barakat A. Serum visfatin and its relation to insulin resistance and inflammation in type 2 diabetic patients with or without macroangio-pathy. Saudi Med J 2008; 29:185–192.

Rosa P, Oliveria C, Gufferida F, Reis A. Visfatin, glucose metabolism and vascular disease: a review of evidence. Diabetol Metab Syndr 2010; 2:21–26.

Shelbaya S, Shoeib N, Seddik S, Makboul K, Abd El Baki R, Fahmy E, El-ghohary E. Study of the adipocytokine visfatin in obesity and type 2 diabetes mellitus. Endocrine 2011; 25:P160.

Pagano C, Pilon C, Olivieri M, Mason P, Fabries R, Serra R, et al. Reduced plasma visfatin/pre-B cell colony enhancing factor in obesity is not related to insulin resistance in human. J Clin Endocrinol Metab 2006; 91: 3165–3170.

Dogru T, Sonmez A, Tasci L, Bozoglo E, Yilmaz M, Genc H, et al. Plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance. Diabetes Res Clin Pract 2007; 76:24–29.

Berndt J, Kloting N, Kralish S, Kovacs P, Fasshauer M, Michael R, et al. Plasma visfatin concentration and fat depot-specific mRNA expression in humans. Diabetes 2005; 54:2911–2916.

Gursoy G, Akcayoz SS, Acar Y, Demirbas B. Visfatin in hyperlipidemic female patients. J Med Med Sci 2010; 1:120–125.

Takebayashi K, Suetsugu M, Wakabayashi S, Aso Y, Inukai T. Association between plasma visfatin and vascular endothelial function in patients with type 2 diabetes mellitus. Metabolism 2007; 56:451–458.