Dyer J, Wood I S, Palejwala A, Ellis A, Shirazi-Beechey S P
Department of Veterinary Preclinical Sciences, The University of Liverpool, Brownlow Hill and Crown Street, Liverpool L69 7ZJ, United Kingdom.
Am J Physiol Gastrointest Liver Physiol. 2002 Feb;282(2):G241-8. doi: 10.1152/ajpgi.00310.2001.
Noninsulin-dependent diabetes mellitus (NIDDM) is an increasingly common disease, which brings a number of life-threatening complications. In rats with experimentally induced diabetes, there is an increase in the capacity of the intestine to absorb monosaccharides. We have examined the activity and the expression of monosaccharide transporters in the intestine of patients suffering from NIDDM. Na(+)-dependent D-glucose transport was 3.3-fold higher in brush-border membrane (BBM) vesicles isolated from duodenal biopsies of NIDDM patients compared with healthy controls. Western analysis indicated that SGLT1 and GLUT5 protein levels were also 4.3- and 4.1-fold higher in diabetic patients. This was associated with threefold increases in SGLT1 and GLUT5 mRNA measured by Northern blotting. GLUT2 mRNA levels were also increased threefold in the intestine of diabetic patients. Analysis of other BBM proteins indicated that the activity and abundance of sucrase and lactase were increased by 1.5- to 2-fold and the level of the structural proteins villin and beta-actin was enhanced 2-fold in diabetic patients compared with controls. The increase in the capacity of the intestine to absorb monosaccharides in human NIDDM is due to a combination of intestinal structural change with a specific increase in the expression of the monosaccharide transporters SGLT1, GLUT5, and GLUT2.
非胰岛素依赖型糖尿病（NIDDM）是一种日益常见的疾病，会引发多种危及生命的并发症。在实验性诱导糖尿病的大鼠中，肠道吸收单糖的能力会增强。我们研究了NIDDM患者肠道中糖转运蛋白的活性和表达情况。与健康对照组相比，从NIDDM患者十二指肠活检标本中分离出的刷状缘膜（BBM）小泡中，依赖钠的D - 葡萄糖转运活性高3.3倍。蛋白质免疫印迹分析表明，糖尿病患者中SGLT1和GLUT5蛋白水平也分别高出4.3倍和4.1倍。通过Northern印迹法检测发现，SGLT1和GLUT5的mRNA水平也增加了3倍。糖尿病患者肠道中GLUT2的mRNA水平同样增加了3倍。对其他BBM蛋白的分析表明，与对照组相比，糖尿病患者中蔗糖酶和乳糖酶的活性及丰度增加了1.5至2倍，而结构蛋白绒毛蛋白和β -肌动蛋白的水平则提高了2倍。人类NIDDM患者肠道吸收单糖能力的增强，是肠道结构变化与单糖转运蛋白SGLT1、GLUT5和GLUT2表达特异性增加共同作用的结果。
