title: The role of aging upon β cell turnover.
abstract: Preservation and regeneration of β cell endocrine function is a long-sought goal in diabetes research. Defective insulin secretion from β cells underlies both type 1 and type 2 diabetes, thus fueling considerable interest in molecules capable of rebuilding β cell secretion capacity. Though early work in rodents suggested that regeneration might be possible, recent studies have revealed that aging powerfully restricts cell cycle entry of β cells, which may limit regeneration capacity. Consequently, aging has emerged as an enigmatic challenge that might limit β cell regeneration therapies. This Review summarizes recent data regarding the role of aging in β cell regeneration and proposes models explaining these phenomena.
authors: McNair Medical Institute, Pediatric Diabetes and Endocrinology, Baylor College of Medicine, Houston, Texas 77030, USA. kushner@bcm.edu
authors: Jake A
authors: JA
authors: Kushner
mesh_terms: D000375:Aging; D000818:Animals; D002453:Cell Cycle / Q000235:genetics; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000502:physiology; D003920:Diabetes Mellitus / Q000473:pathology*; D044127:Epigenesis, Genetic; D006801:Humans; D007328:Insulin / Q000378:metabolism / Q000502:physiology; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000502:physiology*; D008938:Mitosis; D010179:Pancreas / Q000473:pathology / Q000503:physiopathology; D012038:Regeneration
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D007328:Insulin