Conditions

Twin and family studies indicate that genetic factors alone cannot explain the etiology of T1DM. Seasonality, increasing incidence and epidemics of T1DM as well as numerous ecological, cross-sectional and retrospective studies suggest a critical role of environmental factors, such as infections with certain viruses (especially enteric infections in early life) and effects of early childhood diet. Natural history studies that follow children at increased risk of T1DM provide the best opportunity to study environmental triggers.

New management recommendations for the treatment of type 2 diabetes.

Uncontrolled blood glucose seems to increase the risk of brain troubles.

In part 2 of this exclusive interview, Dr. Aaron Vinik shares an update on INGAP research.

The first large-scale studies of the prediction of T1DM relied upon the detection of cytoplasmic islet cell autoantibodies (ICA) assays based on indirect immunofluorescence. High titer cytoplasmic ICA is most often associated with the presence of multiple islet autoantibodies and therefore a high risk of progression to diabetes.

Two pills provided greater glucose-lowering efficacy than three with low hypoglycemia risk.

Healthier lifestyle found to be result of symptom treatment.

Metformin, sulfonylureas, and insulin studied in type 2 patients.

Type 1A diabetes results from a chronic autoimmune destruction of the pancreatic beta cells, probably initiated by exposure of a genetically susceptible individual to some environmental agent(s). This preclinical period is marked by the presence of autoantibodies to pancreatic beta-cell antigens such as insulin, GAD65 (Glutamic Acid Decarboxylase), ICA512 (called also IA-2) or ZnT8 (Zinc Transporter 8), and precedes the onset of hyperglycemia by a few years.

β-cell centric classification of diabetes puts focus on single common denominator of all types.