Abstract：
Prior evidence indicates that individuals with obesity have an accelerated intestinal glucose absorption. This cross-sectional study evaluated whether those with overweight or obesity display higher duodenal protein levels of the glucose carriers sodium-glucose cotransporter 1 (SGLT-1), glucose transporter 2 (GLUT-2), and glucose transporter 5 (GLUT-5).
SGLT-1, GLUT-2, and GLUT-5 protein levels were assessed on duodenal mucosa biopsies of 52 individuals without diabetes categorized on the basis of their BMI as lean, with overweight, or with obesity.
Individuals with overweight and obesity exhibited progressively increased duodenal protein levels of SGLT-1 and GLUT-5 as compared with the lean group. Conversely, no differences in duodenal GLUT-2 abundance were found among the three groups. Univariate analysis showed that SGLT-1 and GLUT-5 protein levels were positively correlated with BMI, waist circumference, 1-hour post-load glucose, fasting and post-load insulin, and insulin secretion and resistance levels. Furthermore, a positive relationship was detected between intestinal GLUT-5 levels and serum uric acid concentrations, a product of fructose metabolism known to be involved in the pathogenesis of obesity and its complications.
Individuals with overweight and obesity display enhanced duodenal SGLT-1 and GLUT-5 abundance, which correlates with increased postprandial glucose concentrations, insulin resistance, and hyperinsulinemia.
SGLT-1, GLUT-2, and GLUT-5 protein levels were assessed on duodenal mucosa biopsies of 52 individuals without diabetes categorized on the basis of their BMI as lean, with overweight, or with obesity.
Individuals with overweight and obesity exhibited progressively increased duodenal protein levels of SGLT-1 and GLUT-5 as compared with the lean group. Conversely, no differences in duodenal GLUT-2 abundance were found among the three groups. Univariate analysis showed that SGLT-1 and GLUT-5 protein levels were positively correlated with BMI, waist circumference, 1-hour post-load glucose, fasting and post-load insulin, and insulin secretion and resistance levels. Furthermore, a positive relationship was detected between intestinal GLUT-5 levels and serum uric acid concentrations, a product of fructose metabolism known to be involved in the pathogenesis of obesity and its complications.
Individuals with overweight and obesity display enhanced duodenal SGLT-1 and GLUT-5 abundance, which correlates with increased postprandial glucose concentrations, insulin resistance, and hyperinsulinemia.
摘要：
目的：先前的证据表明，肥胖个体的肠道葡萄糖吸收加快。这项横断面研究评估了超重或肥胖患者是否表现出更高的葡萄糖载体钠-葡萄糖协同转运蛋白1（SGLT-1）的十二指肠蛋白水平，葡萄糖转运蛋白2（GLUT-2），和葡萄糖转运蛋白5(GLUT-5)。
方法：SGLT-1、GLUT-2和GLUT-5蛋白水平通过对52名没有糖尿病的人进行十二指肠粘膜活检进行评估，超重，或者肥胖。
结果：超重和肥胖个体与瘦肉组相比，表现出SGLT-1和GLUT-5的十二指肠蛋白水平逐渐升高。相反，三组间十二指肠GLUT-2丰度无差异.单因素分析显示SGLT-1和GLUT-5蛋白水平与BMI呈正相关,腰围,负荷后1小时葡萄糖，空腹和负荷后胰岛素，和胰岛素分泌和抵抗水平。此外，肠道GLUT-5水平与血清尿酸浓度呈正相关，一种已知与肥胖及其并发症发病机制有关的果糖代谢产物。
结论：超重和肥胖患者十二指肠SGLT-1和GLUT-5丰度增加，这与餐后葡萄糖浓度增加有关，胰岛素抵抗，和高胰岛素血症.
方法：SGLT-1、GLUT-2和GLUT-5蛋白水平通过对52名没有糖尿病的人进行十二指肠粘膜活检进行评估，超重，或者肥胖。
结果：超重和肥胖个体与瘦肉组相比，表现出SGLT-1和GLUT-5的十二指肠蛋白水平逐渐升高。相反，三组间十二指肠GLUT-2丰度无差异.单因素分析显示SGLT-1和GLUT-5蛋白水平与BMI呈正相关,腰围,负荷后1小时葡萄糖，空腹和负荷后胰岛素，和胰岛素分泌和抵抗水平。此外，肠道GLUT-5水平与血清尿酸浓度呈正相关，一种已知与肥胖及其并发症发病机制有关的果糖代谢产物。
结论：超重和肥胖患者十二指肠SGLT-1和GLUT-5丰度增加，这与餐后葡萄糖浓度增加有关，胰岛素抵抗，和高胰岛素血症.
