Abstract
The pathophysiology of type II DM is complex; in addition to impaired insulin secretion from Beta-cells, reduced insulin sensitivity was found to play a predominant role in the pathogenesis of the disease. Fetuin-A is a hepatic secretory protein that binds the insulin receptor and inhibits insulin action both in vivo and in vitro. Our aim was to investigate whether serum fetuin-A levels predict the incidence of insulin resistance in type II DM. The present study included 40 patients who had type II diabetes mellitus served as patients group and 40 apparently normal individuals served as control group. All patient and control groups were subjected to the following: full medical history and thorough physical examination, fasting & post prandial blood glucose, urea, creatinine, lipid profile, CRP, insulin and fetuin-A. There was highly significant increase in serum insulin, serum fetuin A and HOMA-IR in diabetic group compared with control group. There was significant positive correlation between serum fetuin A and serum insulin, FBG, HbA1c and serum CRP. Also a significant positive correlation between HOMA-IR and serum fetuin A, serum insulin and HbA1c were found. We concluded that fetuin-A may play a role in the pathogenesis of type II DM, and high serum fetuin-A has a strong association with IR and glycemic control in type II diabetic patients. Future studies are recommended to establish the possibility of using fetuin-A as a predictor of insulin resistance in type II diabetic patients.
Highlights
Diabetes mellitus (DM) is one of the most serious diseases [1]
The pathophysiologies of type II DM are reduced insulin sensitivity and increased insulin resistance associated with enhanced hepatic glucose output and impaired insulin secretion due to a progressive decline of b-cell function [2]
Several circulating proteins have been shown to be involved in the regulation of insulin sensitivity, such as fetuin-A, which is an endogenous inhibitor of the insulin-stimulated receptor tyrosine kinase; high levels of fetuin-A are associated with insulin resistance [3,4,5,6]
Summary
Diabetes mellitus (DM) is one of the most serious diseases [1]. The pathophysiologies of type II DM are reduced insulin sensitivity and increased insulin resistance associated with enhanced hepatic glucose output and impaired insulin secretion due to a progressive decline of b-cell function [2].Several circulating proteins have been shown to be involved in the regulation of insulin sensitivity, such as fetuin-A, which is an endogenous inhibitor of the insulin-stimulated receptor tyrosine kinase; high levels of fetuin-A are associated with insulin resistance [3,4,5,6].Fetuin-A located on chromosome 3q27; this region was mapped as a type II DM and metabolic syndrome susceptibility locus [7]. The pathophysiologies of type II DM are reduced insulin sensitivity and increased insulin resistance associated with enhanced hepatic glucose output and impaired insulin secretion due to a progressive decline of b-cell function [2]. Several circulating proteins have been shown to be involved in the regulation of insulin sensitivity, such as fetuin-A, which is an endogenous inhibitor of the insulin-stimulated receptor tyrosine kinase; high levels of fetuin-A are associated with insulin resistance [3,4,5,6]. The pathophysiology of type II DM is complex; in addition to impaired insulin secretion from Beta-cells, reduced insulin sensitivity was found to play a predominant role in the pathogenesis of the disease. Fetuin-A is a hep atic secretory protein that binds the insulin receptor and inhibits insulin action both in vivo and in vitro
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