Stone L A, Weaver V M, Bruns M E, Christakos S, Welsh J
Department of Biochemistry, School of Medicine, University of Ottawa, Ont., Canada.
Ann Nutr Metab. 1991;35(4):196-202. doi: 10.1159/000177645.
Untreated diabetic (BB) rats exhibited compensatory intestinal growth which was associated with hyperplasia and was accompanied by an increase in unoccupied vitamin D receptors. Although vitamin D receptors were increased, low circulating 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] prevented amplification of the action of 1,25(OH)2D3, as evidenced by reductions in calbindin D-9K and alkaline phosphatase activity in the BB rat intestine compared to control. In the kidney, a lesser degree of compensatory growth was observed which was not associated with hyperplasia, and no significant effect of diabetes on vitamin D receptors or calbindin D-28K was observed. These studies suggest tissue-specific changes in 1,25(OH)2D3 metabolism during spontaneous diabetes which may be related to the hyperplasia which occurs during compensatory tissue growth.
未经治疗的糖尿病(BB)大鼠表现出代偿性肠道生长,这与增生有关,并伴有未被占据的维生素D受体增加。尽管维生素D受体增加,但循环中低水平的1,25 - 二羟基维生素D3 [1,25(OH)2D3] 阻止了1,25(OH)2D3作用的放大,与对照组相比,BB大鼠肠道中钙结合蛋白D - 9K和碱性磷酸酶活性降低证明了这一点。在肾脏中,观察到的代偿性生长程度较小,且与增生无关,未观察到糖尿病对维生素D受体或钙结合蛋白D - 28K有显著影响。这些研究表明,自发性糖尿病期间1,25(OH)2D3代谢存在组织特异性变化,这可能与代偿性组织生长过程中发生的增生有关。