title: Repurposing an Osteoporosis Drug for β Cell Regeneration in Diabetic Patients.
abstract: Replenishing the lost or dysfunctional insulin-producing β cell mass in diabetic patients could slow down or reverse disease progression. Kondegowda et al. (2015) now show that osteoprotegerin and denosumab, inhibitors of the receptor activator of the NF-κB Ligand (RANKL) pathway and osteoclast activation, stimulate human β cell proliferation and therefore possess therapeutic potential.
authors.affiliation: Institute of Diabetes and Regeneration Research, Helmholtz Center Munich, Am Parkring 11, 85748 Garching, Germany.
authors.forename: Felizitas
authors.initials: F
authors.lastname: Schmitz
authors.affiliation: Institute of Diabetes and Regeneration Research, Helmholtz Center Munich, Am Parkring 11, 85748 Garching, Germany.
authors.forename: Sara
authors.initials: S
authors.lastname: Roscioni
authors.affiliation: Institute of Diabetes and Regeneration Research, Helmholtz Center Munich, Am Parkring 11, 85748 Garching, Germany; Institute of Stem Cell Research, Helmholtz Center Munich, Am Parkring 11, 85748 Garching, Germany. Electronic address: heiko.lickert@helmholtz-muenchen.de.
authors.forename: Heiko
authors.initials: H
authors.lastname: Lickert
mesh_terms: D000818:Animals; D050071:Bone Density Conservation Agents / Q000494:pharmacology*; D049109:Cell Proliferation / Q000187:drug effects*; D000069448:Denosumab / Q000494:pharmacology*; D006801:Humans; D050417:Insulin-Secreting Cells / Q000187:drug effects*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D053244:Osteoprotegerin / Q000378:metabolism*
chemical_list: D050071:Bone Density Conservation Agents; D016328:NF-kappa B; D053244:Osteoprotegerin; D000069448:Denosumab