Endocrine Abstracts

Type 1 diabetes (T1D) is a chronic disease of childhood that also presents in adults, resulting from the destruction of insulin-producing β-cells by auto-reactive T cells that have escaped central and peripheral immune tolerance. It is now well established that T1D is characterised by a wide heterogeneity especially in terms of age at onset, representing a major barrier for both pathogenesis and translational efforts aimed to develop novel therapeutics approach. This concept represents a key factor in defining who should be treated with an intervention capable of inducing disease remission. The insulin secretory capacity assessed by the residual β-cell function (measurement of C-peptide) at the time of diagnosis and during the first few year after T1D diagnosis is a crucial factor to define when and how to intervene with the aim of modifying the natural history of the disease on the short and long term. We have to remember that in the vast majority of T1D patients at diagnosis a significant mass of functional islets has been destroyed by the autoimmune attack, thus lacking the chance to be either preserved or rescued by a therapeutic approach able to reverse the course of disease onset. However, some T1D patients show a substantial residual β-cell function at diagnosis and also in the first year after disease manifestation, thus representing an interesting population to target for an intervention able to protect endogenous insulin secretion. Furthermore, some patients may be overweight and become insulin resistant, thus implying that also this pathophysiological condition should be tackled. Patients with T1D and substantial residual β-cell function with or without signs of insulin resistance identify a specific endotypes of T1D. These novel concepts pave the way for new and diverse therapeutic options which can be applied to well characterised patients accordingly.