Stio M, Lunghi B, Iantomasi T, Vincenzini M T, Treves C
Department of Biochemical Sciences, University of Florence, Italy.
J Mol Cell Cardiol. 1994 Nov;26(11):1421-8. doi: 10.1006/jmcc.1994.1161.
The purpose of this study was to investigate whether vitamin D3 deficiency and 1,25-dihydroxyvitamin D3 treatment affect some aspects of heart metabolism in the rat. To this end, five experimental groups were studied: (1) the control group of the vitamin D3 supplemented rats (Group A); (2) rachitic rats (Group B); (3) rachitic rats treated with 1,25-dihydroxyvitamin D3 (Group C); (4) rats fed a vitamin D-deficient diet (Group D); (5) rats fed a vitamin D-deficient diet and treated with 1,25-dihydroxyvitamin D3 (Group E). The five groups were compared by checking in the heart some metabolic parameters, i.e. citrate content, and enzyme activities in cytosol and mitochondria. Citrate content was higher in the heart of treated animals when compared with the control. As regards the enzymatic activities in heart mitochondria, NAD(+)-dependent isocitrate dehydrogenase remarkably decreased in Group B rats and 1,25-dihydroxyvitamin D3 restored quite normal values. NADP(+)-dependent isocitrate dehydrogenase decreased in Group B and Group D animals, and 1,25-dihydroxyvitamin D3 treatment was effective in restoring control values. Cytochrome c oxidase activity did not change, while citrate synthase showed an increase in all the treated rats. As regards the cytosolic enzymes, fructose-6-phosphate kinase increased in the two groups of vitamin D-deplete rats in comparison with the control. Glyceraldehyde-3-phosphate dehydrogenase and 3-phosphoglycerate kinase showed a similar trend: an increase in all the treated animals. In heart homogenate, acylphosphatase and acid phosphatase activities were also determined. Acylphosphatase increased in the treated rats, while acid phosphatase decreased in the rats injected with 1,25-dihydroxyvitamin D3. These results support the hypothesis of a participation of 1,25-dihydroxyvitamin D3 in some aspects of heart metabolism.
本研究的目的是调查维生素D3缺乏和1,25 - 二羟基维生素D3治疗是否会影响大鼠心脏代谢的某些方面。为此，研究了五个实验组：（1）补充维生素D3的大鼠对照组（A组）；（2）佝偻病大鼠（B组）；（3）用1,25 - 二羟基维生素D3治疗的佝偻病大鼠（C组）；（4）喂食维生素D缺乏饮食的大鼠（D组）；（5）喂食维生素D缺乏饮食并用1,25 - 二羟基维生素D3治疗的大鼠（E组）。通过检查心脏中的一些代谢参数，即柠檬酸含量以及细胞质和线粒体中的酶活性，对这五组进行了比较。与对照组相比，治疗动物心脏中的柠檬酸含量更高。关于心脏线粒体中的酶活性，B组大鼠中NAD(+)依赖的异柠檬酸脱氢酶显著降低，而1,25 - 二羟基维生素D3使其恢复到相当正常的值。NADP(+)依赖的异柠檬酸脱氢酶在B组和D组动物中降低，1,25 - 二羟基维生素D3治疗有效地恢复了对照值。细胞色素c氧化酶活性没有变化，而柠檬酸合酶在所有治疗大鼠中均显示增加。关于细胞质酶，与对照组相比，两组维生素D缺乏大鼠中的6 - 磷酸果糖激酶增加。甘油醛 - 3 - 磷酸脱氢酶和3 - 磷酸甘油酸激酶呈现相似趋势：所有治疗动物中均增加。在心脏匀浆中，还测定了酰基磷酸酶和酸性磷酸酶活性。治疗大鼠中酰基磷酸酶增加，而注射1,25 - 二羟基维生素D3的大鼠中酸性磷酸酶降低。这些结果支持了1,25 - 二羟基维生素D3参与心脏代谢某些方面的假设。
