Fedorak R N
University of Alberta, Department of Medicine, Edmonton, Canada.
Can J Physiol Pharmacol. 1990 May;68(5):630-5. doi: 10.1139/y90-092.
Intestinal amino acid and glucose transport is increased in various disease states and physiological circumstances. This enhancement is generally due to an increase in transport capacity (Vmax) without a change in carrier affinity (KD). Furthermore, the increase in transport capacity is too large to be attributed, in most cases, to simple intestinal hypertrophy. In the streptozotocin-treated chronically diabetic rat model, specific binding indicated an enhanced total number of glucose carriers in the small intestine compared with controls. Furthermore, autoradiography reveals that specific phlorizin (i.e., glucose) binding extends into the intervillous region of the intestine, while in age-matched controls binding is confined to the villous tip. These studies suggest that during experimental diabetes mellitus in rats, enhanced intestinal nutrient absorption may occur as a consequence of recruitment of carriers into previously nontransporting enterocytes. This review looks at ways in which this alteration may be influenced, and examines the expression of various isoforms of Na-K ATPase during streptozocin-induced diabetes mellitus.
在各种疾病状态和生理情况下，肠道氨基酸和葡萄糖的转运都会增加。这种增强通常是由于转运能力（Vmax）增加而载体亲和力（KD）不变。此外，在大多数情况下，转运能力的增加幅度太大，不能简单地归因于肠道肥大。在链脲佐菌素处理的慢性糖尿病大鼠模型中，特异性结合表明与对照组相比，小肠中葡萄糖载体的总数增加。此外，放射自显影显示，特异性根皮苷（即葡萄糖）结合延伸至肠道绒毛间区域，而在年龄匹配的对照组中，结合局限于绒毛顶端。这些研究表明，在大鼠实验性糖尿病期间，肠道营养物质吸收增强可能是由于载体被招募到先前不进行转运的肠细胞中所致。本综述探讨了这种改变可能受到影响的方式，并研究了链脲佐菌素诱导的糖尿病期间钠钾ATP酶各种同工型的表达。
