title: The effect of insulin and insulin-like growth factor-I on glucose transport in normal and small for gestational age fetal rats.
abstract: In a model of asymmetric small for gestational age (SGA) fetal growth retardation, we have previously found that glucose transport is decreased in lung (an organ whose growth is restricted) and unaffected in brain (growth is normal). The SGA model alters a number of physiological and metabolic factors that may decrease glucose transport, thereby causing growth retardation. Specifically, insulin and insulin-like growth factor-I (IGF-I) concentrations are diminished in SGA fetuses. We hypothesized that the specific modulation by these factors of gene expression of a glucose transporter, Glut-1, is impaired. We performed bilateral uterine arterial ligation in pregnant rats on day 19 of gestation (term = 21.5 days) and obtained fetal brain, lung, and skeletal muscle on day 20. Lung and muscle explants and monolayers of glial cells and type II pneumocytes were cultured in the presence or absence of insulin or IGF-I for 24 h. Glucose uptake and levels of Glut-1 protein and mRNA were similar in brains of SGA and control fetuses and were not affected by treatment with insulin or IGF-I. Treatment with insulin or IGF-I increased glucose uptake and levels of Glut-1 protein and mRNA in a dose-dependent manner in lung and muscle from control fetuses. However, the response in SGA lung was not as great as that in controls. SGA muscle demonstrated no significant response to either hormone. These findings suggest that changes in glucose transport modulation might contribute to the development of asymmetric growth retardation, and that maintenance of normal transporter function and expression in brain may play a role in sparing its growth.
authors.affiliation: Department of Pediatrics, Northwestern University Medical School, Chicago, Illinois.
authors.forename: R A
authors.initials: RA
authors.lastname: Simmons
authors.forename: A S
authors.initials: AS
authors.lastname: Flozak
authors.forename: E S
authors.initials: ES
authors.lastname: Ogata
mesh_terms: D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D001835:Body Weight; D001921:Brain / Q000196:embryology / Q000378:metabolism; D002478:Cells, Cultured; D003847:Deoxyglucose / Q000378:metabolism; D005317:Fetal Growth Retardation / Q000378:metabolism; D005333:Fetus / Q000378:metabolism*; D005865:Gestational Age; D005947:Glucose / Q000378:metabolism*; D051272:Glucose Transporter Type 1; D007328:Insulin / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D008168:Lung / Q000196:embryology / Q000378:metabolism; D009004:Monosaccharide Transport Proteins / Q000235:genetics / Q000378:metabolism; D009132:Muscles / Q000196:embryology / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D051272:Glucose Transporter Type 1; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D012333:RNA, Messenger; C495679:Slc2a1 protein, rat; D007334:Insulin-Like Growth Factor I; D003847:Deoxyglucose; D005947:Glucose