Background: Visceral fat-derived protein named visfatin was discovered in 2005. Visfatin may improve glucose tolerance, and its plasma levels correlate strongly with the amount of visceral adipose tissue in humans. Visfatin has insulin-like metabolic effects on glucose metabolism but has a distinct binding site on insulin receptors. These findings triggered great interest for many researchers to explore the mechanism(s) of regulation of visfatin expression, and the possible relationships between visfatin and obesity, insulin resistance, and T2DM. However, the available information on visfatin is still too little and controversial.
Aim: The aim is to study the levels of visfatin and its relationship to each of obesity, insulin resistance and T2DM.
Subjects and methods: The study was conducted on 80 subjects divided into Group I a: 20 obese T2DM patients, Group I b: 20 lean T2DM patients, Group II a: 20 obese nondiabetic, Group II b: 20 lean nondiabetic subjects. They were subjected to, full clinical history, thorough clinical examination, fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), fasting plasma insulin (FI), homeostasis model assessment (HOMA-IR), cholesterol, TG, LDL-c, HDL-c, serum visfatin and CT abdomen to assess the visceral (VAT) and subcutaneous (SAT) adipose tissue of the patients chosen randomly.
Results: Serum visfatin was found to be higher in T2DM patients than control group as well as in T2DM obese patients than obese control group and in T2DM lean patients than lean control group. Also serum visfatin was higher in obese T2DM patients than T2DM lean patients. There was a highly significant positive correlation (P≤0.001) between serum visfatin and BMI, FPG, HbA1c, TG, cholesterol, HOMA IR and FI and a significant positive correlation (P≤0.05) between visfatin and waist circumference and VAT.
Conclusion: These results may postulate the presence of a link between visfatin and diabetes mellitus independent of obesity.