Although 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.
In this study, 103 Yemeni male subjects aged 25–42 years, with BMI < 25 kg/m 2 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.
Both 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).
Triglyceride 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.