Treatment Options for Type 2 Diabetes in Youth Remain Limited

The incidence and prevalence of type 2 diabetes (T2D) in youth are steadily increasing. The Centers for Disease Control and Prevention recently published the projected prevalence of T2D in youth using the SEARCH for Diabetes in Youth Study database from 2001 for prevalence and 2002 for incidence. Based on these data and assuming a 2.3% increase annually, it is predicted that the prevalence of T2D in youth could quadruple in 40 years. 1 As in adults with T2D, adolescents develop macrovascular and microvascular complications, including albuminuria, hypertension, and dyslipidemia. These complications occur earlier and appear to be more rapidly progressive in youths than in adults. 2 Thus, prevention and treatment of T2D is paramount. Prevention begins with addressing known risk factors for developing T2D, the most important of which is obesity. Most youths with T2D have a body mass index (BMI) greater than the 85th percentile and are diagnosed between the ages of 10 and 16 years, around the time of puberty and the associated physiologic insulin resistance. 3 Occurrence is familial; 74%100% of adolescents with T2D have an affected first or second degreerelative. 4 OtherriskfactorsfordevelopingT2Darelarge forgestationalageorsmallforgestationalagebirthweightsand high risk ethnicities. American Indians are the most affected, followed in decreasing order by African Americans, Hispanics, Asian/Pacific Islanders, and non-Hispanic Whites. 3 Understanding the pathophysiology of diabetes has led to the development of novel treatments. T2D is due to insulin resistance and a relative insulin deficiency due to beta cell dysfunction with eventual beta cell failure. The time to beta cell failure in youth is more rapid than in adulthood, with the rate of beta cell function declining by � 20% per year in 6 youths who underwent clamp studies. 5 Explanations for the beta cell failure include beta cell exhaustion because of increased insulin secretion to compensate for insulin resistance, desensitization of the beta cell because of hyperglycemia (glucotoxicity), lipotoxicity, and a reduction of beta cell mass from amyloid deposition. 6 At diag