Visfatin: Potential Role as Therapeutic Biomarker in Type 2 Diabetes Mellitus
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Abstract
Background: Type 2 Diabetes mellitus (DM) is a group of metabolic diseases characterized by hyperglycemia due to pathophysiologic abnormalities, like insulin resistance, impaired insulin secretion and deregulated hepatic glucose production. Visfatin is an adipokine which acts synergistically with insulin to increase glucose cellular uptake, stimulate glucose transfer to the muscle and adipose tissue and prevents hepatic glucose production. It also upregulates the production of the pro- and anti-inflammatory cytokines such as IL-1β, IL-1Ra, IL-6, IL-10 and TNF-α in human monocytes suggesting a potential role of visfatin in the pathogenesis of vascular inflammation in obesity and type 2 DM.
Materials and Methods: In this study, samples of 90 cases and 90 controls were included. Each sample was tested for fasting plasma glucose, serum lipid profile, serum insulin and serum visfatin. The data were analyzed by unpaired students t-test and linear regression analysis using IBM SPSS version 22 statistics software.
Results: The mean fasting plasma glucose level in control group is 84 ± 14.3 mg/dL and that of cases is 178.8 ± 94.5 mg/dL. The mean serum visfatin level in controls is 104.9 ± 60.2 pg/mL and that of cases is 161.1 ± 79.8 pg/mL. The mean serum fasting insulin in controls is 7.1 ± 4.2 mU/L and that of cases is 11.3 ± 2.6 mU/L. The mean HOMA-IR in controls is 1.8 ± 1.2 and that of cases is 5.1 ± 1.4. We observed a positive correlation (r = 0.833) between serum insulin and serum visfatin, which is statistically significant (p<0.05).
Conclusion: The raised Serum visfatin in Diabetes Mellitus may be a compensatory mechanism to the insulin resistant state present in these patients. Hyperglycemia seen in Diabetes Mellitus stimulates visfatin secretion from adipocytes, which in turn increases glucose-stimulated insulin secretion from beta cells of pancreas, leading to Hyperinsulinemia. But the exact mechanism of its action is still not elucidated.