Editorial - Regulation of Postnatal β Cell Mass

Abstract

Pancreatic cells are responsible for producing all of the insulin required by an organism to maintain glucose homeostasis. Defects in the development, maintenance, or expansion of cell mass can result in diabetes. Current treatments for diabetes primarily focus on replacing insulin (Types 1 and 2 diabetes) and improving cell function (Type 2 diabetes only). However, increasing a patient's own cell mass or preventing cell loss could improve or cure their condition. Currently, efforts are ongoing in several laboratories to differentiate cells from precursor populations and to expand cells in vitro to generate an unlimited supply for transplantation. Theoretically, the same could be done in vivo to regenerate and/or expand a patient's existing cell population. Thus, it is important to understand the molecular regulation of cell mass development, survival, and expansion. cell mass is increased by cell neogenesis (differentiation from precursor cells), cell proliferation, and cell hypertrophy (increased cell size), while cell mass is decreased by cell death and atrophy (decreased cell size). Although it was once thought that cell number did not expand after birth, prevailing evidence now shows that new cells can form throughout life in both rodent models and humans. The primary mechanism by which new cells form during adulthood in the mouse is via proliferation rather than neogenesis, although this is less clear in humans. A reduced cell population at birth may result in fewer cells available to enter the cell cycle later in life, and therefore a reduction in adult cell mass expansion leading to diabetes with age. Under normal circumstances during adulthood, cells are a slowly-renewing population, with steady low levels of proliferation and apoptosis, although cell proliferation normally declines with age. In addition to maintaining cell mass under normal circumstances, an organism must also be able to alter its cell mass in accordance with its requirements for insulin. In states of insulin resistance, such as pregnancy and obesity, cell mass is known to increase, and when compensatory cell mass expansion is inadequate, diabetes ensues. Inherent defects that render cells more susceptible to apoptosis, would also result in a negative balance in cell mass, and could contribute to diabetes risk. This special issue of The Open Endocrinology Journal focuses on our current understanding of the genetics and signaling pathways that augment cell mass and enhance cell survival postnatally. Each of the articles in this issue provides an in-depth review of a different facet of cell …