OBJECTIVE -Previous reports have predicted greater risk of type 1 diabetes among people who were heavier as young children. The Accelerator Hypothesis predicts earlier onset in heavier people, without necessarily a change in risk, and views type 1 and type 2 diabetes as the same disorder of insulin resistance, set against different genetic backgrounds. Insulin resistance is a function of fat mass, and increasing body weight in the industrialized world has been accompanied by earlier presentation (i.e., acceleration) of type 2 diabetes. We wanted to establish whether increasing body weight was also asociated with the earlier presentation of type 1 diabetes, as the Accelerator Hypothesis would predict.RESEARCH DESIGN AND METHODS -The relationships between fatness and age at diagnosis were examined in context of birth weight, weight change since birth, weight at diagnosis, BMI at diagnosis, and BMI 12 months later in 94 children aged 1-16 years (49 boys and 45 girls) presenting for management of acute-onset type 1 diabetes.RESULTS -BMI standard deviation score (SDS) at diagnosis, weight SDS change since birth, and BMI SDS 12 months later were all inversely related to age at presentation (r ϭ Ϫ0.39 to Ϫ0.40, P Ͻ 0.001). The boys were significantly fatter than the girls (BMI SDS 0.56 vs. Ϫ0.08, respectively; P ϭ 0.006) and presented with diabetes at a significantly younger age (6.74 vs. 8.32 years, respectively; P Ͻ 0.05). The sex difference in age at diagnosis, however, disappeared when corrected for BMI (P ϭ 0.31), suggesting that fatness or something related to it was the responsible factor.CONCLUSIONS -The data are consistent with the hypothesis that the age at presentation of type 1 diabetes is associated with fatness. The implications for prevention of type 1 diabetes may be important. Diabetes Care 26:2865-2870, 2003T he prevalence of diabetes is increasing rapidly in industrialized countries. Although most attention has focused on the increase in type 2 diabetes, there has been a parallel increase in type 1 diabetes, which requires explanation (1). Type 2 diabetes is believed to result from the loss of ␤-cell function in association with insulin resistance (2). The Accelerator Hypothesis regards type 1 diabetes in the same way (3).Awareness of overlap between type 1 and type 2 diabetes is not new. There has long been interest in insulin resistance in type 1 diabetes, although related more to its implications for management and outcome than to its pathogenesis (4 -8). The term "type one-and-a-half" diabetes, referring to the progression in some from type 2 to type 1 diabetes, was coined years ago and remains an area of lively debate (9). In a modern context, the increasing difficulty in distinguishing type 1 from type 2 diabetes in obese young people has given rise to the designation "double diabetes," in which recognition is given to the coexistence of autoimmunity and insulin resistance (10).The insulin resistance that underlies type 2 diabetes seems to result mainly from lifestyle factors: weight increase a...

There are clear gender and ethnic differences in percentage body fat in British schoolchildren which may relate to known differences in the risk of type 2 diabetes in adolescence and adulthood. BMI criteria for defining overweight and obesity do not accurately identify ethnic differences in body fat.

No abstract

Metformin therapy has a beneficial treatment effect over placebo for BMI-SDS, fasting glucose, ALT, and ALR ratio at 3 months, with changes in BMI-SDS sustained at 6 months.

Transient neonatal diabetes mellitus (TNDM) is a rare form of childhood diabetes which usually resolves in the first 6 months of life but which predisposes to type 2 diabetes of adult onset. We recently reported paternal uniparental isodisomy of chromosome 6 (UPD6) in two children with TNDM and proposed that there may be an imprinted gene important in the aetiology of diabetes on chromosome 6. We now describe two unrelated families which independently suggest that the gene is imprinted, is paternally expressed and maps to 6q22-q23. One family has a duplication while the other, with familial TNDM, shows linkage to a marker in this region.