Mori H, Kasuga M
Internal Medicine II, Kobe University School of Medicine.
Nihon Rinsho. 1996 Oct;54(10):2795-8.
It is necessary to investigate the pathophysiology of impaired glucose tolerance (IGT) because the number of patients with IGT is larger than that of non-insulin-dependent diabetes mellitus (NIDDM) and the subjects with IGT are more likely to progress to overt NIDDM than those with normal glucose tolerance. IGT is a more heterogeneous state in volving various degrees of beta-cell dysfunction and insulin resistance, compared with NIDDM, therefore the approach to the candidate genes whose mutation increases the risk of developing IGT is with difficulty. We describe the direct screening of candidate genes with molecular biological method involved in insulin action, insulin secretion, obesity and adipocyte function, and the prospect of gene targeting study than can clarify the function of a single candidate gene.
有必要对糖耐量受损（IGT）的病理生理学进行研究，因为IGT患者的数量多于非胰岛素依赖型糖尿病（NIDDM）患者，而且与糖耐量正常者相比，IGT患者更易发展为显性NIDDM。与NIDDM相比，IGT是一种更具异质性的状态，涉及不同程度的β细胞功能障碍和胰岛素抵抗，因此，寻找其突变会增加患IGT风险的候选基因颇具难度。我们描述了用分子生物学方法直接筛选参与胰岛素作用、胰岛素分泌、肥胖及脂肪细胞功能的候选基因，以及有望阐明单个候选基因功能的基因靶向研究。
