OBJECTIVE—This study investigates the annual incidence and clinical characteristics of type 2 diabetes among school-aged children as detected by urine glucose screening from 1974 to 2002 in the Tokyo metropolitan area. RESEARCH DESIGN AND METHODS— In total, 8,812,356 school children were examined for glucosuria. Morning urine was used for the analysis. When the urine was positive for glucose, an oral glucose tolerance test was carried out to confirm diabetes. RESULTS—In all, 232 students were identified to have type 2 diabetes. The overall annual incidence of type 2 diabetes was 2.63/100,000. The annual incidence after 1981 was significantly higher than that before 1980 (1.73 vs. 2.76/100,000, P < 0.0001). The annual incidence was significantly higher for junior high school students compared with primary school students (0.78 vs. 6.43/100,000, P < 0.0001). The overall male-to-female ratio of students with type 2 diabetes was 1.0:1.19 (P = 0.296), but it was 1.0:1.56 (P = 0.278) for primary school students. Overall, 83.4% of children with diabetes were obese (≥20% overweight). However, nonobese girls (<20% overweight) with diabetes accounted for 23.0% of the patients, whereas markedly obese boys (≥40% overweight) accounted for 61.5% of the patients. The frequency of a family history of type 2 diabetes in second- and first-degree relatives was 56.5%. CONCLUSIONS—We confirmed that the incidence of young people with type 2 diabetes increased after 1981 in the Tokyo metropolitan area. The increase in the frequency of this disorder seemed to be strongly related to an increasing prevalence of obesity. Age and genetic susceptibility may be associated with the occurrence of type 2 diabetes.

Rev i ew o f P ri m a ry P r eve n t i o n o fTy p e 2 D i a b ete s i n We s te rn Au s t r a l i a E xe c u t i ve S u m m a ry R E V I E W O F P R I M A RY P R E V E N T I O N O F T Y P E 2 D I A B E T E S I N W E S T E R N A U S T R A L I R E V I E W O F P R I M A RY P R E V E

This study presents the characteristics of 20 children (17 female) with NIDDM who required oral hypoglycemic agent (OHA) therapy. A family history of NIDDM was present in 55%. None had islet cell antibodies (ICA) or glutamic acid decarboxylase (GAD) antibodies. Tolbutamide was the drug of choice; glibenclamide was introduced if glycemic control was not obtained after 2 to 3 months of tolbutamide therapy. Seven of the patients eventually required insulin therapy.

This study evaluated recent changes in the annual incidence of childhood type 2 diabetes in the Tokyo metropolitan area. From 1974 to 2004, a total of 236 students were diagnosed as having type 2 diabetes by the urine glucose screening program at school. The overall incidence of type 2 diabetes was 2.55/100,000. Overall, 83.9% of students with diabetes were obese; junior high school students had a significantly higher incidence than primary school students (0.75 vs. 6.27/100,000). The annual incidences over the 5-yr periods from 1974–2004 were 1.73, 3.23, 3.05, 2.90, 2.70 and 1.41/100,000, respectively. The incidences in 1974–1980 and 2001–2004 were significantly lower than those in 1981–1985, 1986–1990 and 1991–1995, because primary school students in 1974–1980 had a significantly lower incidence (0.27/100,000), and junior high school students in 2001–2004 had a somewhat lower incidence (3.66/100,000) than during 1981–2000. In recent years, Japanese children’s lifestyle and eating habits have gradually improved, and this may have contributed to the trend toward decrease in the incidence of type 2 diabetes in 2001–2004 in the Tokyo metropolitan area.

The Burkitt’s lymphoma (BL) cell line Akata retains the latency I program of Epstein-Barr virus (EBV) gene expression and cross-linking of its surface immunoglobulin G (IgG) by antibodies results in activation of viral replication. When EBV nuclear antigen 2 (EBNA2) was artificially expressed by a constitutive expression vector, the Cp EBNA promoter remained inactive and accordingly the latency III program was not induced. In contrast, expression of LMP2A and activity of the Fp lytic promoter were activated. Consistent with this Fp activity, the rate of spontaneous activation of the EBV replicative cycle was increased significantly, suggesting the possibility that EBNA2 can induce EBV replication. The efficiency of anti-IgG-induced activation of the viral replication was reduced in Akata cells expressing EBNA2. To obtain more direct evidence for EBNA2-induced activation of the EBV replicative cycle, this protein was next expressed by a tetracycline-regulated expression system. EBNA2 was undetectable with low doses (<0.5 μg/ml) of tetracycline, while its expression was rapidly induced after removal of the antibiotic. This induced expression of EBNA2 was immediately followed by expression of EBV replicative cycle proteins in up to 50% of the cells, as shown by indirect immunofluorescence and immunoblot analysis. These results suggest an unexpected potential of EBNA2 to disrupt EBV latency and to activate viral replication.