Insulin and glucose modulate glucose transporter messenger ribonucleic acid expression and glucose uptake in trophoblasts isolated from first-trimester chorionic villi

Gordon, Michael; Zimmerman, Peter D.; Landon, Mark B.; Gabbe, Steven G.; Kniss, Douglas A.

doi:10.1016/0002-9378(95)91332-7

Cited by 49 publications

(36 citation statements)

References 25 publications

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“…Our previous report ) demonstrated a time-dependent increase in glucose uptake in mouse placental cells that was consistent with the data in the present Fig. 1a and with those from human first-trimester chorionic villi (Gordon et al 1995).…”

Section: Discussionsupporting

confidence: 93%

“…A previous study demonstrated that incubation with extremely low concentrations of -glucose (0-18·2 mg/dl) enhanced 2-[ 3 H]deoxy--glucose uptake in human firsttrimester trophoblast-like cells, and that the effects of -glucose on GLUT1 mRNA level paralleled the uptake of 2-[ 3 H]deoxy--glucose (Gordon et al 1995). Other studies, and our data, suggest that the glucose concentration may be a potent regulator of GLUT1 expression in the placental cells.…”

Section: Discussionmentioning

confidence: 99%

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High concentration of glucose decreases glucose transporter-1 expression in mouse placenta in vitro and in vivo

Ogura¹,

Sakata²,

Yamaguchi³

et al. 1999

Journal of Endocrinology

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Facilitative glucose transporter-1 (GLUT1) is expressed abundantly and has an important role in glucose transfer in placentas. However, little is known about the regulation of GLUT1 expression in placental cells. We studied the changes in placental GLUT1 levels in relation to changes in glucose concentration in vitro and in vivo. In in vitro experiments, dispersed mouse placental cells were incubated under control (5·5 mM) and moderately high (22 mM) glucose concentrations, and 2-deoxyglucose uptake into cells was studied on days 1-5 of culture. After 4 days of incubation under both conditions, GLUT1 mRNA and proten levels were examined by Northern and immunoblot analyses. Treatment of cells with 22 mM glucose resulted in a significant decrease in 2-deoxyglucose uptake compared with control, from day 2 to day 5 of culture. Moreover, GLUT1 mRNA and protein levels on day 4 of culture were significantly reduced in cells incubated with 22 mM glucose compared with control. Next, we rendered mice diabetic by administering 200 µg/g body weight streptozotocin (STZ) on day 8 of pregnancy. Animals were killed on day 12 of pregnancy and placental tissues were obtained. [3 H]Cytochalasin B binding study was carried out to assess total GLUTs, and GLUT1 mRNA and protein were measured as above.[3 H]Cytochalasin B binding sites in placentas from STZ-treated mice were significantly less than those in control mice. Northern and immunoblot analyses revealed a significant decrease in GLUT1 mRNA and protein levels in diabetic mice compared with the controls. These findings suggest that the glucose concentration may regulate the expression of placental GLUT1.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

High concentration of glucose decreases glucose transporter-1 expression in mouse placenta in vitro and in vivo

Ogura¹,

Sakata²,

Yamaguchi³

et al. 1999

Journal of Endocrinology

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“…GLUT1 transfers glucose in direct proportion to the glucose concentration gradient within physiological ranges [25]. It has been assumed that the human placenta has a limited role in influencing glucose transport to the fetus; however, there is now evidence that both insulin and glucose can modulate GLUT1 expression (and therefore glucose transport) at the level of the placental trophoblast [26,27,35]. Studies using trophoblast cell cultures found that a hyperglycaemic medium resulted in a reduction in GLUT1 protein expression [35].…”

Section: Discussionmentioning

confidence: 99%

Effects of gestational diabetes on human placental glucose uptake, transfer, and utilisation

et al. 2000

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Both pregestational [1] and gestational diabetes mellitus [2,3] can lead to neonatal macrosomia which is associated with fetal death, prematurity, birth trauma, and neonatal respiratory distress syndrome, hypoglycaemia, polycythaemia, hyperbilirubinaemia, hypocalcaemia, hypomagnesaemia and cardiomyopathy [4±6]. For macrosomic neonates, birth weight has not been consistently shown to positively correlate with the degree of control of maternal blood glucose [7,8], suggesting that factors other than or in addition to maternal blood glucose are associated with adverse clinical outcomes during diabetes in pregnancy.Offspring from pregnant women with diabetes are more likely to develop diabetes mellitus and obesity later in life. This observation and evidence that development of diabetes is more closely related to maternal than paternal health, suggests that the intrauterine environment is possibly of importance [9, 10]. Abstract Aims/hypothesis. Gestational diabetes is associated with complications for the offspring before, during and after delivery. Poor maternal glucose control, however, is a weak predictor of these complications. Given its position at the interface of the maternal and fetal circulations, the placenta possibly plays a crucial part in protecting the fetus from adverse effects from the maternal diabetic milieu. We hypothesised that gestational diabetes may result in changes in placental function, particularly with respect to the uptake, transfer, and/or utilisation of glucose. We aimed to examine glucose transport and utilisation in intact human placental lobules from women with gestational diabetes and those from normal pregnancies. Method. Dual perfusion of an isolated placental lobule was done on placentae from diet treated gestational diabetic (n = 7) and normal pregnant patients (n = 9) using maternal glucose concentrations of 4, 8,

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“…The glucose concentration of the maternal perfusate was maintained at 4 mmol/l for the first 30 min of perfusion, while the lobule was cleared of blood. The maternal glucose concentration was then changed at random to 4,8,16 or 24 mmol/l. After 30 min of perfusion at each of these glucose concentrations, 14 C(U)-d-glucose (1mCi/ml) and 3 H-l-glucose (1mCi/ml) were simultaneously infused into the maternal perfusate at 0.1 ml/min for 21 min.…”

Section: Methodsmentioning

confidence: 99%

“…It has been shown that insulin at physiological concentrations increased the rate of glucose uptake into cultured first trimester trophoblasts by increasing GLUT1 expression [8]. Thus, we hypothesised that exogenous insulin treatment would alter placental glucose transfer to the fetus in GDM patients compared with GDM patients not requiring insulin therapy.…”

mentioning

confidence: 96%

Placental glucose transport and utilisation is altered at term in insulin-treated, gestational-diabetic patients

et al. 2001

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Insulin and glucose modulate glucose transporter messenger ribonucleic acid expression and glucose uptake in trophoblasts isolated from first-trimester chorionic villi

Cited by 49 publications

References 25 publications

High concentration of glucose decreases glucose transporter-1 expression in mouse placenta in vitro and in vivo

High concentration of glucose decreases glucose transporter-1 expression in mouse placenta in vitro and in vivo

Effects of gestational diabetes on human placental glucose uptake, transfer, and utilisation

Placental glucose transport and utilisation is altered at term in insulin-treated, gestational-diabetic patients

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