Serum visfatin in type 2 diabetes mellitus

Abstract

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.