Jean-Pierre Riveline

Prise de position de la Société Francophone du Diabète (SFD) sur la prise en charge médicamenteuse de l'hyperglycémie du patient diabétique de type 2

Composition du groupe de relecture Mme Carole Avril, Directrice Générale de la Fédération Française des Diabétiques (Paris) Dr Éric Drahi, médecin généraliste (Saint-Jean-de-Braye) Pr Jean Doucet, interniste gériatre et diabétologue, Professeur de Thérapeutique (Rouen) Pr Serge Halimi, endocrinologue-diabétologue, Professeur Émérite de Nutrition (Grenoble) Pr Anne-Marie Magnier, Professeur Honoraire de Médecine Générale (Paris, Sorbonne) Dr Laurent Meyer, endocrinologue-diabétologue (Strasbourg) Pr Ronan Roussel, endocrinologue-diabétologue (Paris, Diderot) Dr Pierre Serusclat, endocrinologue-diabétologue (Vénissieux) Pr Charles Thivolet, endocrinologue-diabétologue (Lyon) Composition du groupe de travail de la SFD Pr Bernard Bauduceau (endocrinologuediabétologue, Saint-Mandé), Pr Lyse Bordier (endocrinologue-diabétologue, Saint-Mandé), Pr Bernard Charbonnel (endocrinologue-diabétologue, Nantes), Pr Emmanuel Cosson (endocrinologuediabétologue, Bobigny), Pr Patrice Darmon (endocrinologue-diabétologue, Marseille), Dr Bruno Detournay (CEMKA-EVAL, Bourg-la-Reine), Pr Pierre Fontaine (endocrinologue-diabétologue, Lille), Pr André Grimaldi (endocrinologue-diabétologue, Paris), Pr Pierre Gourdy (endocrinologue-diabétologue, Toulouse), Pr Bruno Guerci (endocrinologue-diabétologue, Nancy), Pr Hélène Hanaire (endocrinologue-diabétologue, Toulouse ; présidente de la SFD), Pr Alfred Penfornis (endocrinologue-diabétologue, Corbeil-Essonnes), Pr André Scheen (endocrinologue-diabétologue, Liège, Belgique).

Adaptive Beta-Cell Neogenesis in the Adult Mouse in Response to Glucocorticoid-Induced Insulin Resistance

Both type 1 and type 2 diabetes are characterized by deficient insulin secretion and decreased β-cell mass. Thus, regenerative strategies to increase β-cell mass need to be developed. To characterize mechanisms of β-cell plasticity, we studied a model of severe insulin resistance in the adult mouse and defined how β-cells adapt. Chronic corticosterone (CORT) treatment was given to adult mice and led to rapid insulin resistance and adaptive increased insulin secretion. Adaptive and massive increase of β-cell mass was observed during treatment up to 8 weeks. β-Cell mass increase was partially reversible upon treatment cessation and reinduced upon subsequent treatment. β-Cell neogenesis was suggested by an increased number of islets, mainly close to ducts, and increased Sox9 and Ngn3 mRNA levels in islets, but lineage-tracing experiments revealed that neoformed β-cells did not derive from Sox9- or Ngn3-expressing cells. CORT treatment after β-cell depletion partially restored β-cells. Finally, β-cell neogenesis was shown to be indirectly stimulated by CORT because serum from CORT-treated mice increased β-cell differentiation in in vitro cultures of pancreatic buds. Altogether, the results present a novel model of β-cell neogenesis in the adult mouse and identify the presence of neogenic factors in the serum of CORT-treated mice.