부산대학교 도서관

Type 1 diabetes is the third most prevalent chronic disease of childhood, affecting up to 0.4% of children in some populations by age 30 years, with an overall lifetime risk of nearly 1% (1, 2). It is believed that a large proportion of cases of type 1 diabetes result from the autoinmmne destruction of the pancreatic β cells, leading to complete dependence on exogenous insulin to regulate blood glucose levels (3). The etiology of type 1 diabetes is only partially characterized, but it is recognized that both genetic and environmental determinants are important in defining disease risk. Type 1 diabetes clusters in families, based on population-based twin and family studies (4) but does not segregate with a known mode of inheritance (5). The incidence and the age at onset of type 1 diabetes in some populations have changed dramatically since 1950 (6-8). These data, coupled with the incomplete concordance for the phenotype in monozygotic twins (30-70%), suggest that the penetrance of type 1 diabetes susceptibility alleles is strongly influenced by environmental factors (4). [ABSTRACT FROM AUTHOR]