Von der Lippe G, Andersen K J, Schjönsby H
Scand J Gastroenterol. 1977;12(2):183-7.
To determine the mechanism by which pancreatic extract (PE) corrects the malabsorption of vitamin B12 in chronic pancreatic insufficiency (CPI), the following hypotheses were investigated: Firstly, PE might stimulate the absorption of vitamin B12 by changing the intestinal pH, secondly PE might stimulate the intestinal uptake of unbound vitamin B12, thirdly PE might abolish the inhibitory effect of vitamin B12 binders on the intestinal uptake of vitamin B12 bound to intrinsic factor (IF). PE had no effect on the pH in the small intestine and did not stimulate the uptake of unbound 57CoB12 by perfused rat intestinal segments. Preincubation of 57CoB12-IF with a non-IF B12-binder from human saliva (R-binder) reduced the uptake of 57CoB12 from 18.5 pg per cm intestine +/- 3.4 S.E.M. to 7.8 +/- 1.6 (p less than 0.02). PE abolished this inhibitory effect (p less than 0.05). The results indicate that PE corrects the malabsorption of vitamin B12 in CPI by an effect on non-IF B12- binders.
为确定胰腺提取物(PE)纠正慢性胰腺功能不全(CPI)时维生素B12吸收不良的机制,对以下假设进行了研究:第一,PE可能通过改变肠道pH值来刺激维生素B12的吸收;第二,PE可能刺激肠道对未结合维生素B12的摄取;第三,PE可能消除维生素B12结合蛋白对与内因子(IF)结合的维生素B12肠道摄取的抑制作用。PE对小肠pH值无影响,也不刺激灌注大鼠肠段对未结合的57CoB12的摄取。57CoB12-IF与来自人唾液的非IF B12结合蛋白(R-结合蛋白)预孵育后,每厘米肠段对57CoB12的摄取量从18.5 pg±3.4 S.E.M.降至7.8±1.6(p<0.02)。PE消除了这种抑制作用(p<0.05)。结果表明,PE通过对非IF B12结合蛋白的作用来纠正CPI中维生素B12的吸收不良。