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Trehalase activity in genetically diabetic mice (serum kidney and liver).

机译:基因型糖尿病小鼠(血清肾脏和肝脏)中的海藻糖酶活性。

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摘要

Trehalase activity was determined in serum, liver, and kidney in alloxan treated Swiss mice and in homozygous (Ob/Ob, Db/Db) and heterozygous (Ob/+, Db/m+) diabetic mice. Both alloxan and genetic diabetic mice exhibited a large increase in serum and liver trehalase activity with no change in kidney trehalase activity. The heterozygotes (Ob/+, Db/m+) showed only a slight increase of enzyme activity. Further quantitative differences were noticed between the genetic and alloxan diabetic animals. The liver enzyme activity increased from 10- to more than 20-fold in the liver of the homozygous Ob/Ob and Db/Db strains and only 3-fold (not significant compared to controls) in the alloxan treated animals. The above results suggest a regulatory relationship between the genes coding for trehalase and the enzymes of glucose metabolism activity involved in the development of the metabolic anomalies of diabetes. The structural gene for trehalase may well have survived elimination of selective pressure during phylogenesis and remained part of a co-regulated group of glucose metabolising enzymes. This could explain its sensitivity to mutations affecting glucose metabolism and its sensitivity to insulin directed regulatory mechanisms.
机译:在用四氧嘧啶治疗的瑞士小鼠以及纯合型(Ob / Ob,Db / Db)和杂合型(Ob / +,Db / m +)糖尿病小鼠中测定血清,肝和肾中的海藻糖酶活性。四氧嘧啶和遗传糖尿病小鼠均表现出血清和肝脏海藻糖酶活性的大幅增加,而肾脏海藻糖酶活性没有变化。杂合子(Ob / +,Db / m +)仅显示酶活性的轻微增加。在遗传动物和四氧嘧啶糖尿病动物之间发现了进一步的定量差异。在纯合的Ob / Ob和Db / Db菌株的肝脏中,肝酶活性从10倍增加到20倍以上,而在四氧嘧啶处理的动物中,肝酶的活性仅增加了3倍(与对照相比不明显)。上述结果表明,编码海藻糖酶的基因与参与糖尿病代谢异常的葡萄糖代谢活性的酶之间存在调节关系。海藻糖酶的结构基因在系统发育过程中可能已经克服了选择压力的消除,并且仍是葡萄糖代谢酶共同调控组的一部分。这可以解释其对影响葡萄糖代谢的突变的敏感性及其对胰岛素指导的调节机制的敏感性。

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