State Key Lab of Food Science and Technology, Jiangnan University, 1800 Lihu Road, 214122, Wuxi, Jiangsu Province, China.
Mol Biol Rep. 2010 Apr;37(4):1867-74. doi: 10.1007/s11033-009-9622-3. Epub 2009 Jul 19.
Long term intake of high-glucose diet (HGD) may induce many diseases such as dyslipidemia, fatty liver and diabetes disease. Most of the research for molecular mechanisms of the association between HGD and the above diseases focus on the metabolism of glucose and lipid. However, there are few studies on molecular mechanism of the effect of HGD on digestion and absorption. We used HGD (containing 20% glucose) to feed C57BL/6J mice for 4 weeks, detected the expressions of 13,098 genes in jejunums of C57BL/6J mice with DNA microarray. Microarray analysis showed the expression of genes related to digestive enzyme, gastrointestinal peptide and nutrient transporters were significantly changed, which indicated that HGD induced the suppression of digestive enzyme gene expression, attenuation of alimentary tract movement and nutrient transportation. In one word, the microarray analysis suggested that HGD impaired the function of digestion and absorption in jejunum of C57BL/6J mice. We validated our microarray findings by conducting real-time RT-PCR assays on selected genes and detecting the activities of disaccharidases such as lactase, maltase and sucrase in jejunum of C57BL/6J mice.
长期摄入高糖饮食（HGD）可能会导致多种疾病，如血脂异常、脂肪肝和糖尿病。大多数关于 HGD 与上述疾病之间关联的分子机制的研究都集中在葡萄糖和脂质的代谢上。然而，关于 HGD 对消化和吸收的影响的分子机制的研究较少。我们用含有 20%葡萄糖的 HGD 喂养 C57BL/6J 小鼠 4 周，用 DNA 微阵列检测 C57BL/6J 小鼠空肠中的 13098 个基因的表达。微阵列分析显示与消化酶、胃肠肽和营养转运体相关的基因表达显著改变，这表明 HGD 诱导消化酶基因表达抑制、消化道运动减弱和营养转运减少。总之，微阵列分析表明 HGD 损害了 C57BL/6J 小鼠空肠的消化和吸收功能。我们通过对选定的基因进行实时 RT-PCR 检测，并检测 C57BL/6J 小鼠空肠中乳糖酶、麦芽糖酶和蔗糖酶等二糖酶的活性，验证了我们的微阵列发现。
