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Expression of genes involved in placental glucose uptake and transport in the nonobese diabetic mouse pregnancy.

Abstract：

OBJECTIVE:Maternal diabetes alters placental glucose metabolism and maternofetal glucose transport. The purpose of this study was to determine whether genes involved in placental glucose uptake and transport were concomitantly altered, resulting in the observed changes in the state of maternal diabetes. STUDY DESIGN:By means of the nonobese diabetic pregnant mouse we examined the expression of placental glucose transporters, hexokinase I, glycogen content, glycogen-regulating enzyme activities in control animals (blood glucose 8.5 +/- 0.2 mmol/L, n = 25), moderate maternal diabetes (blood glucose 10 to 13.9 mmol/L, n = 16), and severe maternal diabetes (blood glucose > 16.7 mmol/L, n = 12). Comparisons by the analysis of variance and the Newman-Keuls test were performed. RESULTS:Although changes in placental glucose transporters and hexokinase I messenger ribonucleic acid levels occurred, neither 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) occurred in the moderately diabetic group, and changes in placental weight (p < 0.05) and fetal glucose levels (p < 0.02) were observed in the severely diabetic group. CONCLUSIONS:Placental glucose transporting and phosphorylating protein levels by themselves do not regulate diabetes-induced fetoplacental alterations. The lack of a protective decline in these proteins may account for the observed fetoplacental adaptations to excess glucose.

journal_name

Am J Obstet Gynecol

journal_title

American journal of obstetrics and gynecology

authors

Devaskar SU,Devaskar UP,Schroeder RE,deMello D,Fiedorek FT Jr,Mueckler M

doi

10.1016/0002-9378(94)90154-6

subject

Has Abstract

pub_date

1994-11-01 00:00:00

pages

1316-23

issue

5

eissn

0002-9378

issn

1097-6868

pii

0002-9378(94)90154-6

journal_volume

171

pub_type

杂志文章

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