Suzuki S
Third Department of Internal Medicine, Tohoku University School of Medicine.
Nihon Rinsho. 1994 Oct;52(10):2606-10.
We clinically characterized 18 diabetic patients in 7 families with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) and mitochondrial DNA mutations of tRNALEU(UUR) (3243), 5 diabetics in a family with myoclonic epilepsy and ragged red fiber (MERRF) and tRNALYS (8344) mutation and 11 diabetics in a family with chronic external ophthalmoplegia (CPEO) and multiple deletions. Insulin secretory capacities were significantly reduced in the mutant relatives, as compared with the non-mutant members. It is speculated that the mutation-induced OPHOS defects in the pancreatic beta- cells might result in insulin secretory defects.
我们对7个患有线粒体脑肌病、乳酸酸中毒和卒中样发作(MELAS)且存在线粒体DNA tRNALEU(UUR)(3243)突变的家族中的18例糖尿病患者、1个患有肌阵挛性癫痫伴破碎红纤维(MERRF)和tRNALYS(8344)突变的家族中的5例糖尿病患者以及1个患有慢性进行性眼外肌麻痹(CPEO)和多处缺失的家族中的11例糖尿病患者进行了临床特征分析。与非突变成员相比,突变亲属的胰岛素分泌能力显著降低。据推测,胰腺β细胞中由突变引起的氧化磷酸化缺陷可能导致胰岛素分泌缺陷。