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Mutational Analysis of the Coding Regiosn of the Genes Encoding nProtein Kinase B-α and -β, Phosphoinositide-Dependent Protein Kinase-1, Phosphatase Targeting to Glycogen, Protein Phosphatase Inhibitor-1, and Glycogenin

机译:编码nProtein激酶B-α和-β,磷酸肌醇依赖性蛋白激酶1,针对糖原的磷酸酶,蛋白磷酸酶抑制剂1和糖原蛋白编码基因编码突变的突变分析

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The finding of a reduced insulin-stimulated glucose uptake and glycogen synthesis in the skeletal muscle of glucose-tolerant first-degree relatives of patients with NIDDM, as well as in cultured fibroblasts and skeletal Muscle cells isolated from NIDDM patients, ahs been Interpreted as evidence for a genetic involvement in The disease. The mode of inheritance of the common Forms of NIDDM is as yet unclear, but the prevailing Hypothesis supports a polygenic model. In the present Study, we tested the hypothesis that the putative inher- Itable defects of insulin-stimulated muscle glycogen Synthesis might be caused by genetic variability in the Genes encoding proteins shown by biochemical evidence To be involved in insulin-stimulated glycogen synthesis In skeletal muscle.
机译:在NIDDM患者的葡萄糖耐量一级亲属的骨骼肌以及从NIDDM患者分离的培养的成纤维细胞和骨骼肌细胞中发现胰岛素刺激的葡萄糖摄取和糖原合成减少的结果,可以作为证据解释。遗传涉及该疾病。 NIDDM常见形式的遗传方式尚不清楚,但普遍的假设支持多基因模型。在本研究中,我们检验了以下假设:胰岛素刺激的肌肉糖原合成的固有固有缺陷可能是由生化证据显示的编码蛋白质的基因中的遗传变异性引起的。该基因参与骨骼肌中胰岛素刺激的糖原合成。

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