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Maternal Epidermal Growth Factor Deficiency Causes Fetal Hypoglycemia and Intrauterine Growth Retardation in Mice: Possible Involvement of Placental Glucose Transporter GLUT3 Expression¹

Department of Obstetrics and Gynecology (Y.K., O.T., Y.T.), The University of Tokyo, Bunkyo-ku, Tokyo 113, Japan; CREST (O.T.), Japan Science and Technology, Kawaguchi, Saitama 350, Japan; Department of Biosignal Research (A.Y.), Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo 173, Japan; Third Department of Internal Medicine (Y.O.), Yamaguchi University, Ube, Yamaguchi 755, Japan; and Department of Anatomy (J.I.), Nippon Medical School, Bunkyo-ku, Tokyo 113, Japan

Address all correspondence and requests for reprints to: Osamu Tsutsumi, M.D., Ph.D., Department of Obstetrics and Gynecology, The University of Tokyo, Bunkyo-ku, Tokyo 113, Japan. E-mail: osamut-tky{at}umin.ac.jp

We investigated the physiological role of epidermal growth factor (EGF) in fetal growth in mice in which midgestational sialoadenectomy induced maternal EGF deficiency. Sialoadenectomy decreased the fetal weight significantly, indicating that maternal EGF deficiency caused intrauterine growth retardation. The weight of the fetal liver in the sialoadenectomized mice was reduced in proportion to the decrease in body weight (82.7 ± 10.2 vs. 70.9 ± 10.9 mg), whereas the brain weight was not reduced. Sialoadenectomy significantly decreased the glucose concentration in fetal plasma (86.0 ± 13.0 vs. 63.0 ± 11.8 mg/dl) without affecting the maternal plasma level of glucose. Transplacental transfer of ³H-2-deoxyglucose was significantly decreased by sialoadenectomy (5.17 ± 1.25 vs. 2.94 ± 1.02%), but transfer of ¹⁴C-aminoisobutyric acid was not affected. Northern blot analysis and in situ hybridization of glucose transporter isoform GLUT1 and GLUT3 messenger RNAs (mRNAs) in placenta revealed that sialoadenectomy significantly reduced the expression of GLUT3 mRNA without affecting GLUT1 mRNA levels. Administration of anti-EGF antiserum enhanced the effects of EGF deficiency, which were almost completely corrected by EGF supplementation. These results indicate that EGF plays an important role in fetal growth by regulating the transplacental supply of glucose via GLUT3 expression in the placenta.

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