TY - JOUR
T1 - Intra-uterine growth restriction differentially regulates perinatal brain and skeletal muscle glucose transporters
AU - Sadiq, H. Farouk
AU - Das, Utpala G.
AU - Tracy, Thomas F.
AU - Devaskar, Sherin U.
N1 - Funding Information:
This work was supported by Fleur-de-Lis Funds, St. Louis, MO (H.F.S.), NIH-HD33997 (S.U.D.) and the Twenty-five Club Neonatal Research Funds, Magee-Womens Hospital, Pittsburgh, PA. We thank Dr. Mike Mueckler (Washington University, St. Louis, MO) for the anti-Glut 1 and anti-Glut 4 antibodies used in this study. We acknowledge the technical assistance of Rhonda Taylor.
PY - 1999/3/27
Y1 - 1999/3/27
N2 - Employing Western blot analysis, we investigated the effect of maternal uterine artery ligation causing uteroplacental insufficiency with asymmetrical intrauterine growth restriction (IUGR) upon fetal (22d) and postnatal (1d, 7d, 14d and 21d) brain (Glut 1 and Glut 3) and skeletal muscle (Glut 1 and Glut 4) glucose transporter protein concentrations. IUGR was associated with a ~ 42% decline in fetal plasma glucose (p < 0.05) and a ~ 25% decrease in fetal body weights (p < 0.05) with no change in brain weights when compared to the sham operated controls (SHAM). In addition, IUGR caused a ~ 45% increase in fetal brain Glut 1 (55 kDa) with no change in Glut 3 (50 kDa) protein concentrations. This fetal brain. Glut 1 change persisted, though marginal, through postnatal suckling stages of development (1d-21d), with no concomitant change in brain Glut 3 levels at day 1. In contrast, in the absence of a change in fetal skeletal muscle Glut 1 levels (48 kDa), a 70% increase was observed in the 1d IUGR with no concomitant change in either fetal or postnatal Glut 4 levels (45 kDa). The change in skeletal muscle Glut 1 levels normalized by d7 of age. We conclude that IUGR with hypoglycemia led to a compensatory increase in brain and skeletal muscle Glut 1 concentrations with a change in the brain preceding that of the skeletal muscle. Since Glut 1 is the isoform of proliferating cells, fetal brain weight changes were not as pronounced as the decline in somatic weight. The increase in Glut 1 may be protective against glucose deprivation in proliferating fetal brain cells and postnatal skeletal myocytes which exhibit 'catch-up growth', thereby preserving the specialized function mediated by Glut 3 and Glut 4 towards maintaining the intracellular glucose milieu.
AB - Employing Western blot analysis, we investigated the effect of maternal uterine artery ligation causing uteroplacental insufficiency with asymmetrical intrauterine growth restriction (IUGR) upon fetal (22d) and postnatal (1d, 7d, 14d and 21d) brain (Glut 1 and Glut 3) and skeletal muscle (Glut 1 and Glut 4) glucose transporter protein concentrations. IUGR was associated with a ~ 42% decline in fetal plasma glucose (p < 0.05) and a ~ 25% decrease in fetal body weights (p < 0.05) with no change in brain weights when compared to the sham operated controls (SHAM). In addition, IUGR caused a ~ 45% increase in fetal brain Glut 1 (55 kDa) with no change in Glut 3 (50 kDa) protein concentrations. This fetal brain. Glut 1 change persisted, though marginal, through postnatal suckling stages of development (1d-21d), with no concomitant change in brain Glut 3 levels at day 1. In contrast, in the absence of a change in fetal skeletal muscle Glut 1 levels (48 kDa), a 70% increase was observed in the 1d IUGR with no concomitant change in either fetal or postnatal Glut 4 levels (45 kDa). The change in skeletal muscle Glut 1 levels normalized by d7 of age. We conclude that IUGR with hypoglycemia led to a compensatory increase in brain and skeletal muscle Glut 1 concentrations with a change in the brain preceding that of the skeletal muscle. Since Glut 1 is the isoform of proliferating cells, fetal brain weight changes were not as pronounced as the decline in somatic weight. The increase in Glut 1 may be protective against glucose deprivation in proliferating fetal brain cells and postnatal skeletal myocytes which exhibit 'catch-up growth', thereby preserving the specialized function mediated by Glut 3 and Glut 4 towards maintaining the intracellular glucose milieu.
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U2 - 10.1016/S0006-8993(99)01145-2
DO - 10.1016/S0006-8993(99)01145-2
M3 - Article
C2 - 10095016
AN - SCOPUS:0033608783
VL - 823
SP - 96
EP - 103
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -