title: The required beta cell research for improving treatment of type 2 diabetes.
abstract: In healthy individuals, insulin resistance is associated with physiological conditions such as pregnancy or body weight gain and triggers an increase in beta cell number and insulin secretion capacity to preserve normoglycaemia. Failure of this beta cell compensation capacity is a fundamental cause of diabetic hyperglycaemia. Incomplete understanding of the molecular mechanisms controlling the plasticity of adult beta cells mechanisms and how these cells fail during the pathogenesis of diabetes strongly limits the ability to develop new beta cell-specific therapies. Here, current knowledge of the signalling pathways controlling beta cell plasticity is reviewed, and possible directions for future research are discussed.
authors.affiliation: Center for Integrative Genomics, University of Lausanne, Switzerland. Bernard.Thorens@unil.ch
authors.forename: B
authors.initials: B
authors.lastname: Thorens
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000503:physiopathology* / Q000628:therapy*; D018450:Disease Progression; D005260:Female; D005768:Gastrointestinal Hormones / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D008297:Male; D011247:Pregnancy; D012307:Risk Factors; D015398:Signal Transduction
chemical_list: D005768:Gastrointestinal Hormones; D007328:Insulin; D005947:Glucose
keywords: GLP-1; apoptosis; beta cells; diabetes; insulin secretion; pregnancy