Morettini Micaela, Di Nardo Francesco, Ingrillini Laura, Fioretti Sandro, Göbl Christian, Kautzky-Willer Alexandra, Tura Andrea, Pacini Giovanni, Burattini Laura
Department of Information Engineering, Università Politecnica delle Marche, Ancona, Italy.
Department of Obstetrics and Gynecology, Division of Obstetrics and Feto-maternal Medicine, Medical University of Vienna, Vienna, Austria.
Eur J Clin Invest. 2019 Jun;49(6):e13099. doi: 10.1111/eci.13099. Epub 2019 Mar 20.
Obesity is known to induce a deterioration of insulin sensitivity (S ), one of the insulin-dependent components of glucose tolerance. However, few studies investigated whether obesity affects also the insulin-independent component, that is glucose effectiveness (S ). This cross-sectional study aimed to analyse S and its components in different body mass index (BMI) categories.
Three groups of subjects spanning different BMI (kg m ) categories underwent a 3-h frequently sampled intravenous glucose tolerance test: Lean (LE; 18.5 ≤ BMI < 25, n = 73), Overweight (OW; 25 ≤ BMI < 30, n = 90), and Obese (OB; BMI ≥ 30, n = 41). OB has been further divided into two subgroups, namely Obese I (OB-I; 30 ≤ BMI < 35, n = 27) and Morbidly Obese (OB-M; BMI ≥ 35, n = 14). Minimal model analysis provided S and its components at zero (GEZI) and at basal (BIE) insulin.
Values for S were 1.98 ± 1.30 × 10 ·min in all subjects grouped and 2.38 ± 1.23, 1.84 ± 0.82, 1.59 ± 0.61 10 ·min in LE, OW and OB, respectively. In all subjects grouped, a significant inverse linear correlation was found between the log-transformed values of S and BMI (r = -0.3, P < 0.0001). S was significantly reduced in OW and OB with respect to LE (P < 0.001) but no significant difference was detected between OB and OW (P = 0.35) and between OB-I and OB-M (P = 0.25). Similar results were found for GEZI. BIE was not significantly different among NW, OW and OB (P = 0.11) and between OB-I and OB-M (P ≥ 0.07).
S and its major component GEZI deteriorate in overweight individuals compared to those in the normal BMI range, without further deterioration when BMI increases above 30 kg m .
众所周知，肥胖会导致胰岛素敏感性（S）下降，胰岛素敏感性是糖耐量中依赖胰岛素的组成部分之一。然而，很少有研究调查肥胖是否也会影响不依赖胰岛素的组成部分，即葡萄糖效能（S）。这项横断面研究旨在分析不同体重指数（BMI）类别中的S及其组成部分。
三组不同BMI（kg/m²）类别的受试者接受了3小时频繁采样的静脉葡萄糖耐量试验：瘦组（LE；18.5≤BMI＜25，n = 73）、超重组（OW；25≤BMI＜30，n = 90）和肥胖组（OB；BMI≥30，n = 41）。OB组进一步分为两个亚组，即肥胖I组（OB-I；30≤BMI＜35，n = 27）和病态肥胖组（OB-M；BMI≥35，n = 14）。最小模型分析提供了零胰岛素（GEZI）和基础胰岛素（BIE）状态下的S及其组成部分。
所有分组受试者的S值为1.98±1.30×10⁻⁴·min⁻¹，LE组、OW组和OB组的S值分别为2.38±1.23、1.84±0.82、1.59±0.61×10⁻⁴·min⁻¹。在所有分组受试者中，S的对数转换值与BMI之间存在显著的负线性相关（r = -0.3，P＜0.0001）。与LE组相比，OW组和OB组的S显著降低（P＜0.001），但OB组与OW组之间（P = 0.35）以及OB-I组与OB-M组之间（P = 0.25）未检测到显著差异。GEZI也得到了类似结果。NW组、OW组和OB组之间以及OB-I组与OB-M组之间的BIE无显著差异（P = 0.11和P≥0.07）。
与正常BMI范围的个体相比，超重个体的S及其主要组成部分GEZI会下降，而当BMI增加到30kg/m²以上时不会进一步恶化。
