TY - JOUR
T1 - Preserved pancreatic β-cell development and function in mice lacking the insulin receptor-related receptor
AU - Kitamura, T.
AU - Kido, Y.
AU - Nef, S.
AU - Merenmies, J.
AU - Parada, L. F.
AU - Accili, D.
PY - 2001
Y1 - 2001
N2 - Receptors of the insulin/insulinlike growth factor (IGF) family have been implicated in the regulation of pancreatic β-cell growth and insulin secretion. The insulin receptor-related receptor (IRR) is an orphan receptor of the insulin receptor gene (Ir) subfamily. It is expressed at considerably higher levels in β cells than either insulin or IGF-1 receptors, and it has been shown to engage in heterodimer formation with insulin or IGF-1 receptors. To address whether IRR plays a physiologic role in β-cell development and regulation of insulin secretion, we have characterized mice lacking IRR and generated a combined knockout of Ir and Irr. We report that islet morphology, β-cell mass, and secretory function are not affected in IRR-deficient mice. Moreover, lack of IRR does not impair compensatory β-cell hyperplasia in insulin-resistant Ir+/- mice, nor does it affect β-cell development and function in Ir-/- mice. We conclude that glucose-stimulated insulin secretion and embryonic β-cell development occur normally in mice lacking Irr.
AB - Receptors of the insulin/insulinlike growth factor (IGF) family have been implicated in the regulation of pancreatic β-cell growth and insulin secretion. The insulin receptor-related receptor (IRR) is an orphan receptor of the insulin receptor gene (Ir) subfamily. It is expressed at considerably higher levels in β cells than either insulin or IGF-1 receptors, and it has been shown to engage in heterodimer formation with insulin or IGF-1 receptors. To address whether IRR plays a physiologic role in β-cell development and regulation of insulin secretion, we have characterized mice lacking IRR and generated a combined knockout of Ir and Irr. We report that islet morphology, β-cell mass, and secretory function are not affected in IRR-deficient mice. Moreover, lack of IRR does not impair compensatory β-cell hyperplasia in insulin-resistant Ir+/- mice, nor does it affect β-cell development and function in Ir-/- mice. We conclude that glucose-stimulated insulin secretion and embryonic β-cell development occur normally in mice lacking Irr.
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U2 - 10.1128/MCB.21.16.5624-5630.2001
DO - 10.1128/MCB.21.16.5624-5630.2001
M3 - Article
C2 - 11463843
AN - SCOPUS:0034941125
SN - 0270-7306
VL - 21
SP - 5624
EP - 5630
JO - Molecular and cellular biology
JF - Molecular and cellular biology
IS - 16
ER -