When the skeleton is controlling pancreatic β-cell mass during development and after

摘要

The understanding of the phenomenon leading to pancreatic Beta-cell mass regulation represents a critical step in the development of regenerative therapy for diabetic patients. Type 1 (T1D) and type 2 (T2D) diabetes are characterized by a near-absolute or a relative deficiency of Beta-cells numbers, respectively. In T1D, at the time of clinical diagnosis, approximately 60-80 of the insulin-producing cells have been destroyed (1). With the currently available treatments, patients with T1D and T2D develop severe long-term complications that clearly reduce their life expectancy (2-4). While insulin replacement continues to be the primary treatment, the need to establish a precise and physiological gluco-regulation in order to avoid complications has led to multiple avenues of alternative interventions.