title: Resting beta-cells - A functional reserve?
abstract: Pancreatic beta-cells play a pivotal role to synthesize and secrete insulin, as the solo source of the body. Physical as well as functional loss of beta-cells over a certain threshold result in diabetes. While the mechanisms underlying beta-cell loss in various types of diabetes have been extensively studied, less is known about residual beta-cells, found even in autoimmune type 1 diabetes and type 2 diabetes with a substantial amount. Why have these beta-cells been spared? Some patients with neonatal diabetes have demonstrated the life-changing restoration of functional beta-cells that were inactive for decades but awakened in several weeks following specific treatment. The recent striking outcomes of bariatric surgery in many obese diabetic patients indicate that their beta-cells are likely "preserved" rather than irreversibly lost even in the multifactorial polygenic state that is type 2 diabetes. Collectively, the preservation of residual beta-cells in various diabetic conditions challenges us regarding our understanding of beta-cell death and survival, where their sustenance may stem from the existence of resting beta-cells under physiological conditions. We posit that beta-cells rest and that studies of this normal feature of beta-cells could lead to new approaches for potentially reactivating and preserving beta-cell mass in order to treat diabetes.
authors.affiliation: Department of Medicine, The University of Chicago, 5841, South Maryland avenue, MC1027, 60637 Chicago, IL, USA. Electronic address: mhara@uchicago.edu.
authors.forename: M
authors.initials: M
authors.lastname: Hara
authors.affiliation: Department of Medicine, The University of Chicago, 5841, South Maryland avenue, MC1027, 60637 Chicago, IL, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Fowler
authors.affiliation: Department of Medicine, The University of Chicago, 5841, South Maryland avenue, MC1027, 60637 Chicago, IL, USA.
authors.forename: G I
authors.initials: GI
authors.lastname: Bell
authors.affiliation: Department of Medicine, The University of Chicago, 5841, South Maryland avenue, MC1027, 60637 Chicago, IL, USA.
authors.forename: L H
authors.initials: LH
authors.lastname: Philipson
mesh_terms: D000818:Animals; D002452:Cell Count; D002453:Cell Cycle; D019610:Cytoprotection; D003922:Diabetes Mellitus, Type 1 / Q000473:pathology*; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000473:pathology* / Q000502:physiology*; D012038:Regeneration / Q000502:physiology
chemical_list: D007328:Insulin
keywords: Beta-cells; Islet; Pancreas; Resting beta-cells