There are modifiable and unmodifiable risk factors for youth type 2 diabetes (T2DM). Unmodifiable risk factors include genetics/epigenetics, minority race/ethnicity, and puberty. The major modifiable risk factors for youth T2DM are obesity and lifestyle habits of excess nutritional intake and decreased energy expenditure. Thus, in making a clinical diagnosis of T2DM, the major diagnostic criterion, at least in North America and Europe, is overweight/obesity. However, with the increasing rates of obesity in children with autoimmune type 1 diabetes (T1DM) and individuals with MODY, the clinical distinction between youth with T2DM and obese youth with autoimmune T1DM or MODY is difficult and imperfect. The distinction between youth with T2DM and T1DM is further blurred because, not infrequently, youth with T2DM present with diabetic ketoacidosis. Several hypotheses and terminologies have been proposed, such as hybrid diabetes, double diabetes, diabetes type 1.5, and latent autoimmune diabetes of youth, to refer to this subset of young patients with a clinical phenotype consistent with T2DM and evidence of autoimmunity consistent with T1DM. While laboratory assessment for islet autoimmunity could be of value to distinguish the different types of childhood diabetes, currently available commercial assays are not always sufficiently sensitive to detect low antibody titers, yielding negative results when in fact the patient may have autoimmune diabetes.
This lecture will present a pathophysiological perspective to unravel the differences in insulin sensitivity and b-cell function characteristic of each type of diabetes despite obesity changing the face of childhood diabetes. Moreover, novel data with respect to longitudinal changes in the pathophysiological alterations of glucose homeostasis distinctive for each may further clarify this heterogeneous picture.
19 - 21 Sep 2019
European Society for Paediatric Endocrinology