Kaul P, Sidhu H, Sharma S K, Nath R
Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
J Am Coll Nutr. 1996 Jun;15(3):295-302. doi: 10.1080/07315724.1996.10718601.
Calculogenic potential of refined sugars galactose and fructose was examined in vitamin B6 deficient and control rats in terms of their capacity to increase urinary excretion of lithogens.
Male albino rats were fed vitamin B6 deficient diet with 51.7% sucrose+ starch or galactose or fructose as the source of carbohydrate. Pair-fed controls were maintained for all the groups for a period of four weeks. Twenty-four hour urine samples obtained at weekly intervals were analyzed for creatinine, calcium, oxalate, phosphate and uric acid. Microscopic urinalysis was performed at the end of the study.
Urinary calcium excretion increased with respect to baseline in all groups except vitamin B6 control group. On day 28, galactose and fructose-fed rats demonstrated significant hypercalciuria as compared to the sucrose + starch fed group. Vitamin B6 deficient rats (irrespective of the sugar fed) excreted significantly greater urinary calcium compared to pair-fed controls. Oxalate excretion was significantly increased in rats fed galactose compared to those fed fructose or sucrose + starch. Vitamin B6 deficiency further increased oxalate excretion by 1.5, 1.9 and 1.7 fold in sucrose + starch, fructose or galactose fed animals, respectively. Urinary uric acid excretion was enhanced only in fructose-fed rats. There was no change in urinary excretion of creatinine and phosphate in different experimental and control groups. Increased urinary saturation with lithogens caused pronounced crystalluria in all the vitamin B6 deficient groups as well as galactose control group.
The results suggest galactose ingestion is associated with a greater propensity to form calcium oxalate kidney stones than fructose. Calculogenic potential of galactose and fructose is further enhanced in vitamin B6 deficiency.
从增加致石物质尿排泄的能力方面,研究精制糖半乳糖和果糖在维生素B6缺乏及对照大鼠中的产石潜力。
雄性白化大鼠喂以含51.7%蔗糖+淀粉或半乳糖或果糖作为碳水化合物来源的维生素B6缺乏饮食。为所有组维持配对喂养的对照组四周。每周采集的24小时尿液样本分析肌酐、钙、草酸盐、磷酸盐和尿酸。研究结束时进行显微镜下尿液分析。
除维生素B6对照组外,所有组的尿钙排泄相对于基线均增加。在第28天,与蔗糖+淀粉喂养组相比,半乳糖和果糖喂养的大鼠表现出显著的高钙尿症。维生素B6缺乏的大鼠(无论喂养何种糖)与配对喂养的对照组相比,尿钙排泄显著增加。与喂食果糖或蔗糖+淀粉的大鼠相比,喂食半乳糖的大鼠草酸盐排泄显著增加。维生素B6缺乏使蔗糖+淀粉、果糖或半乳糖喂养的动物草酸盐排泄分别进一步增加1.5倍、1.9倍和1.7倍。仅在果糖喂养的大鼠中尿尿酸排泄增加。不同实验组和对照组的肌酐和磷酸盐尿排泄无变化。致石物质导致的尿饱和度增加在所有维生素B6缺乏组以及半乳糖对照组中引起明显的结晶尿。
结果表明,摄入半乳糖比摄入果糖更易形成草酸钙肾结石。在维生素B6缺乏时,半乳糖和果糖的产石潜力进一步增强。