Distinct and Overlapping Functions of Insulin and IGF-I Receptors
Jun Nakae,
Yoshiaki Kido and
Domenico Accili
Naomi Berrie Diabetes Center (J.N., D.A.), Department of Medicine,
College of Physicians & Surgeons of Columbia University, New York, New
York 10032; and Second Department of Internal Medicine (Y.K.), Kobe
University School of Medicine, Kobe 650-0017, Japan
Correspondence: Address all correspondence and requests for reprints to: Domenico Accili, M.D., Berrie Research Pavilion, 1150 Saint Nicholas Avenue, Room 238A, New York, New York 10032. E-mail:
da230{at}columbia.edu
Targeted gene mutations have established distinct, yet overlapping,
developmentalroles for receptors of the insulin/IGF family. IGF-I
receptormediates IGF-I and IGF-II action on prenatal growth and IGF-I
actionon postnatal growth. Insulin receptor mediates prenatal growth
inresponse to IGF-II and postnatal metabolism in response to insulin.
Inrodents, unlike humans, insulin does not participate in embryonic
growthuntil late gestation. The ability of the insulin receptor toact
as a bona fide IGF-II-dependent growth promoter is underscoredby its
rescue of double knockout Igf1r/Igf2r mice. Thus, IGF-II
isa true bifunctional ligand that is able to stimulate both insulin
andIGF-I receptor signaling, although with different potencies.In
contrast, the IGF-II/cation-independent mannose-6-phosphatereceptor
regulates IGF-II clearance. The growth retardationof mice lacking
IGF-I and/or insulin receptors is due to reducedcell number, resulting
from decreased proliferation. Evidencefrom genetically engineered mice
does not support the view thatinsulin and IGF receptors promote
cellular differentiation invivo or that they are
required for early embryonic development.The phenotypes of insulin
receptor gene mutations in humansand in mice indicate important
differences between the developmentalroles of insulin and its receptor
in the two species.
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