p27 Regulates the Transition of β-Cells From Quiescence to Proliferation

• DOI: 10.2337/db06-0249
• Publication Date: 2006-10-25T17:32:13Z
• Authors: Senta Georgia; Anil Bhushan
• Keywords: BETA (programming language)

Diabetes results from an inadequate mass of functional beta-cells. Such inadequacy could result loss beta-cells due to immune assault or the inability compensate for insulin resistance. Thus, mechanisms that regulate number will be key understanding both pathogenesis diabetes and developing therapies. In this study, we show cell cycle regulator p27 plays a crucial role in establishing formed before birth. We accumulates terminally differentiated during embryogenesis. Disabling allows newly are normally quiescent embryogenesis reenter proliferate. As consequence, excess generated p27(-/-) mice, doubling their beta-cell at The early postnatal expansion was unaffected indicating main function is maintain state expanded accompanied by increased secretion; however, mice were glucose intolerant, as these insensitive. To assess affect regeneration models diabetes, injected with streptozotocin (STZ). contrast control displayed elevated blood levels, showed decreased susceptibility develop STZ-induced diabetes. Furthermore, retained ability far greater frequency after compared wild-type littermates. These data indicate important target facilitating therapies