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Department of Physiology (N.D., D.W., A.B.), Southern Illinois University, Carbondale, Illinois 62901-6512 and Edison Biotechnology Institute and Department of Biomedical Sciences (K.T.C., J.J.K.), Ohio University College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701
Address all correspondence and requests for reprints to: Andrzej Bartke, Southern Illinois University School of Medicine, Department of Physiology, Life Science 2, Room 245, Carbondale, Illinois 62901-6512.
Mice homozygous for targeted disruption of the GH receptor/GH binding protein gene (GH-R-KO mice; -/-) exhibit reduced plasma IGF-I levels, elevated plasma GH levels, and dwarf phenotype. Although most GH-R-KO mice are fertile, age at first conception is greatly delayed in -/- x -/- matings. Here we report that the age of vaginal opening is significantly delayed in GH-R-KO vs. normal mice, but it can be advanced by treatment with recombinant human (rh)IGF-I. In pregnant GH-R-KO females, fetal size is reduced and pregnancy is prolonged while placental weight is, unexpectedly, increased. Alterations in fetal and placental weight are related to maternal rather than fetal genotype. Moreover, litter size and body weight of newborn pups are significantly reduced in GH-R-KO vs. normal females. Reduction in litter size reflects both dam and sire effects. We conclude that GH resistance and consequent reduction in peripheral IGF-I levels is associated with delay of female puberty, alterations in fetal and placental growth, delay of parturition, and reduced litter size.
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