Warden R A, Strazzari M J, Dunkley P R, O'Loughlin E V
Faculty of Medicine and Health Sciences, The University of Newcastle, Callaghan, NSW, Australia.
J Nutr. 1996 Jul;126(7):1817-26. doi: 10.1093/jn/126.7.1817.
This study investigated the effect of clinical and subclinical vitamin A deficiency on intestinal structure and function in rats. Weanling male rats fed a vitamin A-deficient diet (VA-) for 40-42 or 60-63 d were compared with rats either pair-fed (PF) or with free access to the same diet supplemented with vitamin A (VA+). A reference (REF) group was fed a standard rat diet. Weight began to plateau in VA- rats after 42 d, becoming significantly different from PF rats at 60-63 d (P < 0.02). Diarrhea did not develop in any study group. VA- rats had clinical signs of vitamin A deficiency in the 60-63 d study, but not in the 40-42 d study. However, serum and liver retinol concentrations were negligible in all VA- rats. VA- rats in the 60-63 d study had significantly reduced villus height (P < 0.02), and sucrase and maltase activities (P < 0.02) compared with PF rats. There were no differences between VA- and PF rats in mucosal wet weights, protein and DNA concentrations, thymidine kinase activity and glucose transport. No differences were detected in the 40-42 d study for any variable measured. Because clinical vitamin A deficiency in rats causes only mild changes in intestinal structure and function, it is unlikely that these alterations alone are responsible for the interactions observed in epidemiological studies between vitamin A deficiency and diarrheal disease.
本研究调查了临床和亚临床维生素A缺乏对大鼠肠道结构和功能的影响。将断奶雄性大鼠分为三组,分别给予维生素A缺乏饮食(VA-)40 - 42天或60 - 63天,与配对喂养(PF)或自由获取添加维生素A的相同饮食(VA+)的大鼠进行比较。另设一个参考(REF)组,给予标准大鼠饮食。VA-组大鼠体重在42天后开始趋于平稳,在60 - 63天时与PF组大鼠体重有显著差异(P < 0.02)。各研究组均未出现腹泻。在60 - 63天的研究中,VA-组大鼠出现了维生素A缺乏的临床症状,但在40 - 42天的研究中未出现。然而,所有VA-组大鼠的血清和肝脏视黄醇浓度均极低。在60 - 63天的研究中,与PF组大鼠相比,VA-组大鼠的绒毛高度显著降低(P < 0.02),蔗糖酶和麦芽糖酶活性也显著降低(P < 0.02)。VA-组和PF组大鼠在黏膜湿重、蛋白质和DNA浓度、胸苷激酶活性及葡萄糖转运方面无差异。在40 - 42天的研究中,所测的任何变量均未发现差异。由于大鼠临床维生素A缺乏仅导致肠道结构和功能的轻微变化,因此这些改变不太可能单独导致在流行病学研究中观察到的维生素A缺乏与腹泻病之间的相互作用。