Serum Visfatin, Insulin Resistance and Beta Cell Function in Type Ii Diabetic Patients and Non-Diabetic Adult Offspring With Positive Parental History of Type Ii Diabetes Mellitus

Abstract

Introduction:
 Non-diabetic individuals with type II diabetic parents are more susceptible to develop Diabetes. Visfatin; an adipocytokine and an enzyme is linked with glucose metabolism and affected by obesity. It works like insulin in the human body. It serves as a key enzyme in nicotinamide adenine dinucleotide biosynthesis and plays a pivotal role in glucose mediated insulin secretion.
 Aims and Objectives: In this study we aimed to determine and compare serum visfatin levels, insulin resistance (HOMA-IR) and beta cell function (HOMA-%B) of type II diabetic patients and non-diabetic adult offspring of type II diabetic parents with that of non-diabetic adult offspring of non-diabetic parents.
 Material and methods
 It was a cross-sectional comparative study conducted at Diabetes clinic of Lahore General Hospital (LGH) and department of Physiology, Post Graduate Medical Institute (PGMI), Lahore in 2018. The study groups included thirty type II diabetic subjects (group III) and forty non-diabetic adult offspring of type II diabetic parents (group II). Forty non-diabetic adult offspring of non-diabetic parents served as controls (group I). The subjects were of thirty to fifty years of age. Blood pressure, BMI and waist circumference of every subject was measured. Fasting blood samples of the subjects were analyzed for serum insulin, glucose and visfatin. Insulin resistance (HOMA-IR), insulin sensitivity (HOMA-%S) and beta cell function (HOMA-%β) were also calculated.
 Results
 Type II diabetics (group III) had significantly higher serum visfatin, HOMA-IR, and lower HOMA-%S as compared to the controls (group I). No significant difference was found between HOMA-%B of group III and controls. On the contrary, non-diabetic adult offspring of type II diabetic parents (group II) had significantly lower serum visfatin and HOMA-%S while HOMA-%β, HOMA-IR was significantly higher in comparison to the control group (group I).
 Conclusion
 Visfatin production seems suppressed in non-diabetic individuals with type II diabetic parents probably due to hyperinsulinemia. Moreover, it has a little role in insulin secretion in these individuals as reflected by their higher HOMA-%B index. However, visfatin’s upregulation in chronic hyperglycemia is indicative of its restorative role in the declined beta-cell function in type II diabetics.