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Am J Physiol Endocrinol Metab 278: E127-E133, 2000;
0193-1849/00 $5.00
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Vol. 278, Issue 1, E127-E133, January 2000

Mice lacking insulin receptor substrate 4 exhibit mild defects in growth, reproduction, and glucose homeostasis

Valeria R. Fantin, Qing Wang, Gustav E. Lienhard, and Susanna R. Keller

Department of Biochemistry, Dartmouth Medical School, Hanover, New Hampshire 03755

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 ~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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