Stone L A, Weaver V M, Bruns M E, Welsh J
Dept of Biochemistry, Faculty of Medicine, University of Ottawa, Ontario, Canada.
Diabetes Res. 1990 Dec;15(4):165-72.
Our data confirms previous reports of intestinal and kidney compensatory growth, low plasma 1,25(OH)2D3 and up regulation of intestinal VDRs during untreated diabetes. All of these parameters were normalized in diabetic rats treated with exogenous insulin. There were no alterations in VDR numbers in kidneys or thymus of untreated diabetic animals, indicating that up-regulation of VDRs during untreated diabetes did not occur in all vitamin D target tissues. Compensatory growth of the intestine during untreated diabetes was associated with both hypertrophy and hyperplasia, whereas diabetic kidney growth appeared to be associated with hypertrophy without hyperplasia. Diabetes did not affect somatic index of thymus. The data suggests that the up regulation of VDRs during untreated diabetes may be unique to the intestine and further that VDR up regulation may be related to hyperplasia. Calbindin D-9K was significantly lower in diabetic intestine, suggesting that low circulating 1,25(OH)2D3 prevented amplification of 1,25(OH)2D3's action despite up regulation of intestinal VDRs.
我们的数据证实了先前有关未经治疗的糖尿病期间肠道和肾脏代偿性生长、血浆1,25(OH)₂D₃水平降低以及肠道维生素D受体（VDR）上调的报道。在用外源性胰岛素治疗的糖尿病大鼠中，所有这些参数均恢复正常。未经治疗的糖尿病动物的肾脏或胸腺中VDR数量没有变化，这表明未经治疗的糖尿病期间VDR的上调并非在所有维生素D靶组织中都发生。未经治疗的糖尿病期间肠道的代偿性生长与肥大和增生均有关，而糖尿病肾脏的生长似乎仅与肥大有关，无增生。糖尿病不影响胸腺的躯体指数。数据表明，未经治疗的糖尿病期间VDR的上调可能是肠道特有的，进一步表明VDR上调可能与增生有关。糖尿病肠道中钙结合蛋白D-9K显著降低，这表明尽管肠道VDR上调，但循环中低水平的1,25(OH)₂D₃阻止了1,25(OH)₂D₃作用的放大。
