Department of Biochemistry and Molecular Biology, Faculty of Medicine and Health Sciences, University of Sana'a, Sana'a, Republic of Yemen.
BMC Endocr Disord. 2021 Jun 16;21(1):124. doi: 10.1186/s12902-021-00788-5.
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 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; 6.0 × 10; 6.6 × 10; 1.3 × 10; 5.5 × 10, 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; B = 0.024, p = 1.05 × 10), HOMA-β (B = 16.8, p = 6.8 × 10; B = 0.95, p = 0.004), insulin (B = 16.5, p = 1.2 × 10; B = 1.19, p = 8.3 × 10) 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.
尽管有大量证据表明,2 型糖尿病患者的一级亲属(FDRs)中胰岛素抵抗(HOMA-IR)和β细胞功能障碍(HOMA-β)的相对贡献,但很少有研究报告 HOMA-IR 和 HOMA-β与代谢综合征之间的关联。我们的目的是评估代谢综合征因素对非糖尿病 2 型糖尿病患者 FDRs 的 HOMA-IR、HOMA-β 和糖蛋白的影响。
本研究共检查了 103 名也门男性,年龄在 25-42 岁之间,BMI<25kg/m,其中 39 名为无糖尿病家族史的正常对照组,64 名为 2 型糖尿病患者的非糖尿病 FDRs。
非糖尿病 FDRs 的糖蛋白、糖化血红蛋白(HbA1c)和果糖胺以及胰岛素、HOMA-IR 和 HOMA-β均显著升高(p=4.9×10;6.0×10;6.6×10;1.3×10;5.5×10,分别),与对照组相比。空腹血糖虽然在正常范围内,但在非糖尿病 FDRs 中显著升高(p=0.026)。线性回归分析显示,TG 和 WC 是显著增加 HOMA-IR(B=0.334,p=1.97×10;B=0.024,p=1.05×10)、HOMA-β(B=16.8,p=6.8×10;B=0.95,p=0.004)、胰岛素(B=16.5,p=1.2×10;B=1.19,p=8.3×10)和 HbA1c(B=0.001,p=0.034;B=0.007,p=0.037)的主要代谢综合征因素。
在 2 型糖尿病患者的非糖尿病 FDR 男性中,甘油三酯和 WC 是与胰岛素抵抗、基础β细胞功能和胰岛素水平相关的重要代谢综合征因素。此外,FDRs 表现出胰岛素抵抗和代偿性β细胞功能(高胰岛素血症),这表明在 2 型糖尿病风险个体中,胰岛素抵抗先于胰腺β细胞功能障碍的发展。