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  • Title: Mice lacking insulin receptor substrate 4 exhibit mild defects in growth, reproduction, and glucose homeostasis.
    Author: Fantin VR, Wang Q, Lienhard GE, Keller SR.
    Journal: Am J Physiol Endocrinol Metab; 2000 Jan; 278(1):E127-33. PubMed ID: 10644546.
    Abstract:
    The insulin receptor substrates (IRSs) function in insulin signaling. Four members of the family, IRS-1 through IRS-4, are known. Previously, mice with targeted disruption of the genes for IRS-1, -2, and -3 have been characterized. To examine the physiological role of IRS-4, we have generated and characterized mice lacking IRS-4. Male IRS-4-null mice were approximately 10% smaller in size than wild-type male mice at 9 wk of age and beyond, whereas the female null mice were of normal size. Breeding pairs of IRS-4-null mice reproduced less well than wild-type mice. IRS-4-null mice exhibited slightly lower blood glucose concentration than the wild-type mice in both the fasted and fed states, but the plasma insulin concentrations of the IRS-4-null mice in the fasted and fed states were normal. IRS-4-null mice also showed a slightly impaired response in the oral glucose tolerance test. Thus the absence of IRS-4 caused mild defects in growth, reproduction, and glucose homeostasis.
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