Abstract

Abstract The protection of intrinsic factor by vitamin B 12 was demonstrated by testing the effect of the presence of B 12 during procedures known to inactivate intrinsic factor. Intrinsic factor was measured in vivo by its effect on the absorption of B 12 . The presence of B 12 also prevented destruction of B 12 binding sites measured in vitro by dialysis. Instillation of B 12 in the stomach of rats after ligation of the pylorus enhanced the yield of rat intrinsic factor. Exposure of human gastric juice in vitro to autogenous digestion, digestion by added pepsin, heating, and storage also showed that B 12 protects human intrinsic factor against these damaging procedures. Increasing the time of incubation at 37 °C. of fresh gastric juice caused progressive loss of intrinsic factor, which could partially be prevented by B 12 . The presence of B 12 during heating at 50 ° and 58 °C. prevented the otherwise rapid inactivation of intrinsic factor at these temperatures for at least 2 hours. At 65 °C., free intrinsic factor was inactivated within minutes, but the B 12 intrinsic factor complex was less labile. At room temperature, B 12 binding of acid gastric juice diminished gradually over a period of 3 days but was stable when B 12 had been added. Loss of B 12 binding was always reflected by loss of in vivo activity, but the latter might be depressed relatively more than the binding. It is suggested that the protective effect of vitamin B 12 on intrinsic factor is an important physiologic defense against autogenous digestion and that achlorhydria may be viewed as a desirable feature in patients whose gastric atrophy is sufficient to cause serious lack of intrinsic factor.

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