Emerging Epidemic of type 2 diabetes in youth

This review considers the epidemiologic evidence for an increasing incidenc e of type 2 diabetes in youth, the classification and diagnostic issues rel ated to diabetes in young populations, pathophysiologic mechanisms relevant to the increasing incidence, the role of genetics and environment, and the community challenge for prevention and treatment. Type 2 diabetes in youth has been recognized to be frequent in populations of native Noah Americans and to comprise some 30 percent of new cases of diabetes in the 2nd decade of life, largely accounted for by minority populations and associated with obesity Among Japanese schoolchildren, type 2 diabetes is seven times more common than type 1, and its incidence has increased more than 30-fold over the past 20 years, concomitant with changing food patterns and increasing obesity rates. The forms of diabetes seen in children and youth include typ ical type 1, occurring in all races; type 2, seen predominantly in minority youth; atypical diabetes, seen as an autosomal dominantly transmitted diso rder in African-American populations; and maturity-onset diabetes of the yo ung (MODY), seen rarely and only in Caucasians. Of the nonautoimmune forms of diabetes seen in youth, only type 2 diabetes is increasing in incidence. Proper classification requires consideration of onset (acute/severe versus insidious), ethnicity family history presence of obesity and if necessary, studies of diabetes-related autoimmunity. Insulin resistance predicts the development of diabetes in Pima Indians, in offspring of parents with type 2 diabetes, and in other high-risk populations. African-American children a nd youth have greater insulin responses during glucose tolerance testing an d during hyperglycemic clamp study than do whites. There is also evidence o f altered beta-cell function preceding the development of hyperglycemia. Of particular interest is the evidence that abnormal fetal and infantile nutr ition is associated with the development of type 2 diabetes in adulthood. T he thrifty phenotype hypothesis states that poor nutrition in fetal and inf ant life is detrimental to the development and function of the beta-cells a nd insulin sensitive tissues, leading to insulin resistance under the stres s of obesity The thrifty genotype hypothesis proposes that defective insuli n action in utero results in decreased fetal growth as a conservation mecha nism, but at the cost of obesity induced diabetes in later childhood or adu lthood. The vast majority of type 2 diabetes in adults is polygenic and ass ociated with obesity Monogenic forms (MODY, maternally transmitted mitochon drial mutations) are rare, but are more likely to appear in childhood. Link age studies of the common polygenic type 2 diabetes have emphasized the het erogeneity of the disorder. The prevention and treatment of type 2 diabetes in children and youth is a daunting challenge because of the enormous beha vioral influence, difficulty in reversing obesity; and typical nonadherence in this age-group. The emerging epidemic of type 2 diabetes in the pediatr ic population, especially among minorities whose proportion in the U.S. pop ulation is increasing, presents a serious public health problem. The full e ffect of this epidemic will be felt as these children become adults and dev elop the long-term complications of diabetes.