Van Wouwe J P, Uijlenbroek J J
Drechtsteden Hospital Jacobus, Zwijndrecht, The Netherlands.
Biol Trace Elem Res. 1994 Aug;42(2):143-9. doi: 10.1007/BF02785385.
A low Zn diet resulted in subacute Zn deficiency in young rats. Thirty minutes after the intubation of a trace 65-Zn we determined the total tissue Zn activity in plasma, erythrocytes, liver, pancreas, bone, muscle, and proximal jejunum. Assuming the body behaved like a closed multicompartmental system in steady state, we estimated the initial Zn exchange between plasma, and the erythrocytes or these tissues. In comparison with control animals the exchanges between plasma and erythrocytes or pancreas increased threefold during subacute Zn deficiency. In the pancreas the ratio also reversed from < 1.0 to > 1.0. This confirmed earlier observations that the specific activity (kBq 65-Zn/mol Zn) increased mostly in the pancreas. By increased net Zn uptake during subacute deficiency, the pancreas Zn content remained constant in chronic Zn deficiency. We discussed the regulation of the Zn status by the pancreas. We hypothesize that the exocrine pancreas modulates Zn absorption by an exocrine ligand that enhances absorption in the jejunum during subacute deficiency: Unsaturated with Zn it binds dietary intraluminal Zn and increases the Zn absorption. The literature provides evidence in confirmation. This hypothesis explains also conflicting data on the inherited Zn malabsorption syndrome Acrodermatitis Enteropathica.
低锌饮食导致幼鼠出现亚急性锌缺乏。在微量65锌插管30分钟后，我们测定了血浆、红细胞、肝脏、胰腺、骨骼、肌肉和空肠近端组织中的总锌活性。假设身体在稳态下表现为一个封闭的多室系统，我们估计了血浆与红细胞或这些组织之间的初始锌交换。与对照动物相比，亚急性锌缺乏期间血浆与红细胞或胰腺之间的交换增加了三倍。在胰腺中，该比值也从<1.0 逆转至>1.0。这证实了早期的观察结果，即比活性（kBq 65锌/摩尔锌）主要在胰腺中增加。通过亚急性缺乏期间锌净摄取的增加，胰腺锌含量在慢性锌缺乏时保持恒定。我们讨论了胰腺对锌状态的调节。我们假设外分泌胰腺通过一种外分泌配体调节锌的吸收，该配体在亚急性缺乏期间增强空肠中的吸收：未与锌饱和时，它结合膳食腔内锌并增加锌的吸收。文献提供了证实的证据。这一假设也解释了遗传性锌吸收不良综合征肠病性肢端皮炎的相互矛盾的数据。
