When the Skeleton Is Controlling Pancreatic β-Cell Mass During Development and After

  1. Bruno Lefebvre2,3
  1. 1Laboratory of Cell Biology, Institute of Life Science, Catholic University of Louvain, Louvain-la-Neuve, Belgium
  2. 2Université Lille Nord de France, Lille, France
  3. 3Alzheimer and Tauopathies, Jean-Pierre Aubert Research Center, INSERM UMR837, Lille, France
  1. Corresponding author: Bruno Lefebvre, bruno.lefebvre{at}inserm.fr.

The understanding of the phenomenon leading to pancreatic β-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 β-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 (24). While insulin replacement continues to be the primary treatment, the need to establish a precise and physiological glucoregulation in order to avoid complications has led to multiple avenues of alternative interventions. Some studies fulfilled this requirement with allogenic transplantation of human islets or insulin-producing cells (5,6). Still under extensive study, the use of pig islets as an alternative source of insulin-producing cells for xenotransplantation seems to be promising and could represent the future of cell therapy for diabetes (7). Other studies have aimed at abrogating the cause of the disease (i.e., the autoimmunity leading to the destruction of β-cells in T1D) (8). Finally, others worked on the reestablishment of an adequate β-cell mass able to restore euglycemia through methods that promote β-cell preservation and/or regeneration in diabetic individuals (9– …

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