Abstract

BackgroundAlthough there is abundant evidence indicating the relative contribution of insulin resistance (HOMA-IR) and β-cell dysfunction (HOMA-β) among first-degree relatives (FDRs) of Type 2 DM patients, few studies reported the association between HOMA-IR and HOMA-β with metabolic syndrome. Our objective was to evaluate the impact of metabolic syndrome factors on HOMA-IR, HOMA-β and glycoproteins in non-diabetic FDRs.MethodsIn this study, 103 Yemeni male subjects aged 25–42 years, with BMI < 25 kg/m2 were examined, 39 of whom were normal subjects with no family history of diabetes served as control and 64 subjects were non-diabetic FDRs of Type 2 DM patients.ResultsBoth glycoproteins, glycated haemoglobin (HbA1c) and fructosamine as well as insulin, HOMA-IR and HOMA-β were significantly (p = 4.9 × 10−9; 6.0 × 10−8; 6.6 × 10−12; 1.3 × 10−7; 5.5 × 10−12, respectively) higher in non-diabetic FDRs as compared to control group. Fasting plasma glucose, though within normal range, were significantly (p = 0.026) higher in non-diabetic FDRs. Linear regression analysis showed that both TG and WC are the main metabolic syndrome factors that significantly increased HOMA-IR (B = 0.334, p = 1.97 × 10−6; B = 0.024, p = 1.05 × 10−5), HOMA-β (B = 16.8, p = 6.8 × 10−5; B = 0.95, p = 0.004), insulin (B = 16.5, p = 1.2 × 10−6; B = 1.19, p = 8.3 × 10−6) and HbA1c (B = 0.001, p = 0.034; B = 0.007, p = 0.037).ConclusionTriglyceride and WC are the important metabolic syndrome factors associated with insulin resistance, basal β-cell function and insulin levels in non-diabetic FDR men of Type 2 DM patients. Moreover, FDRs showed insulin resistance with compensatory β-cell function (hyperinsulinaemia) suggesting that insulin resistance precede the development of pancreatic β-cell dysfunction in individuals at risk of Type 2 DM.

Highlights

  • There is abundant evidence indicating the relative contribution of insulin resistance (HOMAIR) and β-cell dysfunction (HOMA-β) among first-degree relatives (FDRs) of Type 2 Diabetes Mellitus (DM) patients, few studies reported the association between homeostasis model assessment of insulin resistance (HOMA-IR) and β-cell function (HOMA-β) with metabolic syndrome

  • The results presented in this study showed that TG and Waist circumference (WC) are the main metabolic syndrome factors that increased insulin resistance, β-cell function, insulin and Glycated haemoglobin (HbA1c) in non-diabetic FDRs of Type 2 DM

  • Our results revealed that non-diabetic FDRs of Type 2 DM patients to have insulin resistance and no signs of impaired β-cell function as reflected by the significantly higher HOMA-IR (87.5%) and HOMA-β (37.7%) with respect to the control subjects; suggesting that insulin resistance precedes the development of pancreatic βcell dysfunction in individuals at risk of developing Type 2 DM

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Summary

Introduction

There is abundant evidence indicating the relative contribution of insulin resistance (HOMAIR) and β-cell dysfunction (HOMA-β) among first-degree relatives (FDRs) of Type 2 DM patients, few studies reported the association between HOMA-IR and HOMA-β with metabolic syndrome. Type 2 DM is a heterogeneous group of disorders that display relative insulin deficiency and is usually associated with obesity, insulin resistance, impaired insulin secretion, and increased hepatic glucose production [2]. Both genetic susceptibility and environmental factors likely contribute to the development of Type 2 DM [3]. Longitudinal studies of individuals that developed Type 2 DM showed a rise in insulin levels in the normoglycaemic and pre-diabetic phases that maintain glycaemia near normal despite the presence of insulin resistance (β-cell compensation), followed by a decline in insulin levels (βcell dysfunction) when fasting glycaemia exceeds the upper limit of normal [4]

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