EXPRESSION OF GENES INVOLVED IN PLACENTAL GLUCOSE-UPTAKE AND TRANSPORT IN THE NONOBESE DIABETIC MOUSE PREGNANCY

OBJECTIVE: Maternal diabetes alters placental glucose metabolism and m aternofetal glucose transport. The purpose of this study was to determ ine whether genes involved in placental glucose uptake and transport w ere concomitantly altered, resulting in the observed changes in the st ate of maternal diabetes. STUDY DESIGN: By means of the nonobese diabe tic pregnant mouse we examined the expression of placental glucose tra nsporters, hexokinase I, glycogen content, glycogen-regulating enzyme activities in control animals (blood glucose 8.5 +/- 0.2 mmol/L, n = 2 5), moderate maternal diabetes (blood glucose 10 to 13.9 mmol/L, n = 1 6), and severe maternal diabetes (blood glucose > 16.7 mmol/L, n = 12) . Comparisons by the analysis of variance and the Newman-Keuls test we re performed. RESULTS: Although changes in placental glucose transport ers and hexokinase I messenger ribonucleic acid levels occurred, neith er state of diabetes altered the corresponding protein levels. Changes in placental deoxyribonucleic acid (p < 0.05) and glycogen content (p < 0.01), fetal insulin levels (p < 0.02), and fetal size (p < 0.05) o ccurred in the moderately diabetic group, and changes in placental wei ght (p < 0.05) and fetal glucose levels (p < 0.02) were observed in th e severely diabetic group. CONCLUSIONS: Placental glucose transporting and phosphorylating protein levels by themselves do not regulate diab etes-induced fetoplacental alterations. The lack of a protective decli ne in these proteins may account for the observed fetoplacental adapta tions to excess glucose.