ESPE Abstracts

Double diabetes (DD) is a term coined to describe individuals with evidence of islet-cell autoimmunity (type 1 diabetes: T1D) and showing obesity and insulin resistance (type 2 diabetes: T2D). The rising obesity trend that favors insulin resistance seems have a role, in association with other environmental factors, for the development of islet-cell autoimmunity through different mechanism. It has become apparent that more youth with T1D are overweight or even obese before hyperglycemia develop. Therefore, diagnosis of T1D is not easy to place because the phenotypic manifestations typically coincident with T2D. In addition, obesity may contribute to the escalation of beta-cell distraction, as suggested by the accelerate hypothesis in individuals generally suspected as T1DM. Insulin resistance not only accelerates the apoptosis of beta cells but also renders them more immunogenic. Genetic factors associate with obesity also accelerates beta-cell function failure. In many cases, common pathogenic processes in T1D and T2D may be evident. SEARCH reported that youth diagnosed with T1D, who had autoantibodies to beta cells, exhibited a higher prevalence of overweight, but not obesity, than nondiabetic youths (1). Gluffrida et al. (2) reported that one-third of patients with T1D had overweight/obese during follow-up, and we also found 27% of those had BMI more than 25 during follow-up. Increasing tendency of childhood overweight/obese worldwide may contribute to increase the number of DD.

Therapeutic approach for DD should include lifestyle modifications, including diet and physical activities. High-dose insulin due to insulin resistance may aggravate overweight/obese. Some oral hypoglycemic drugs, such as metformin and SGLT2 inhibitors, can be used in combination with insulin therapy. We experienced effectiveness of these drugs, which improved glycemic control with reductions of body weight and insulin doses in some cases.

References: 1) Pediat Diabetes 2010;11:4, 2) Diabetol Metab Syndr 2016;8:23