Ultrastructural Localization of Insulin Receptors in Human Placenta

Jones, Carolyn M.; Hartmann, Michaele; Blaschitz, Astrid; Desoyé, Gernot

doi:10.1111/j.1600-0897.1993.tb00614.x

Cited by 41 publications

(18 citation statements)

References 20 publications

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“…Although placentas have abundant insulin binding sites ( Jones et al 1993), it has been accepted that the placenta is insulin-insensitive for glucose transport (Challier et al 1986), which is consistent with our data (Fig. 5).…”

Section: Discussionsupporting

confidence: 83%

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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: 83%

“…Placental glucose transport has been suggested to be independent of insulin stimulation (Challier et al 1986), in spite of the presence of large amounts of placental insulin receptors ( Jones et al 1993). Therefore, we investigated the effect of 1 and 5 µg/ml insulin on glucose uptake by placental cells.…”

Section: Resultsmentioning

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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“…If so, it could explain why placental growth is only retarded in poorly or uncontrolled first trimester diabetic pregnancies, implying some compensatory growth later on. Alternatively, the hyperglycaemia-induced growth arrest of trophoblasts and placenta and, hence, fetus could be released in vivo by fetally derived insulin, which can bind to the cytotrophoblast [28].…”

Section: Discussionmentioning

confidence: 99%

Hyperglycaemia in vitro alters the proliferation and mitochondrial activity of the choriocarcinoma cell lines BeWo, JAR and JEG-3 as models for human first-trimester trophoblast

Weiß¹,

Červar²,

Puerstner³

et al. 2001

Diabetologia

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Despite considerable advances in the treatment of diabetes in the past decades, diabetic pregnancies can still be associated with fetal growth disturbances even when an optimized and intensive metabolic control has been achieved. Macrosomia of the fetus is a common and well-known consequence of maternal diabetes with an increased obstetric risk. The increase in fetal fat mass that accounts for the fetal overweight [1] is the result of fetal hyperinsulinism as a consequence of maternal and, therefore, fetal hyperglycaemia [2]. According to the dynamics of fetal growth, macrosomia is caused by metabolic alterations or hyperglycaemic insults predominantly in later stages of pregnancy [3,4]. In contrast diabetes-associated metabolic derangements in the first trimester of pregnancy can lead to malformations [5] and to delayed growth of the developing embryo [6,7]. Whereas the molecular mechanisms underlying embryo malformations have received enormous attention, no data are available to explain early fetal growth delay. Because of the close link between placental and fetal growth, early intrauterine growth delay could be caused by a reduced growth of the pla- Diabetologia (2001) Abstract Aims/hypothesis. Early intrauterine growth delay in diabetes could be caused by a reduced growth of the placenta. Our study investigates whether hyperglycaemia in vitro reduces trophoblast proliferation. Methods. First-trimester trophoblast cell models (BeWo, JAR and JEG-3 choriocarcinoma cells) were cultured for 24 and 48 h with 5.5 mmol/l d-glucose, 25 mmol/l d-glucose (hyperglycaemia) and with an osmotic control. Cell number, total protein and nucleic acid content and mitochondrial activity (tetrazolium salt assay) were measured, the cell cycle analysed (FACS, cyclin B1 levels) and apoptosis (Annexin-V) measured.Results. In BeWo cells hyperglycaemia reduced cell number, protein, nucleic acid and cyclin B1 levels. The reduced G 2 /M and increased G 0 /G 1 population after 24 h reflects growth arrest at G 0 /G 1 . In JAR cells after 24 h the population was arrested in G 0 /G 1 , whereas after 48 h the G 0 /G 1 block was abrogated and the cells were arrested at G 2 /M. The net effect was an unchanged cell number. In JEG-3 cells hyperglycaemia resulted in fewer cells after 24 h but not after 48 h indicating some adaptation. Mitochondrial activity was either stimulated (BeWo) or reduced (JAR, JEG-3) under hyperglycaemia. Some of these effects were also induced by hyperosmolarity alone. Conclusion/interpretation. Hyperglycaemia has the potential to inhibit the proliferation of first-trimester trophoblast cell models. The mechanisms leading to growth arrest and to changes in mitochondrial activity are complex and depend on differentiation. We hypothesise a hyperglycaemia-induced impairment of placental growth in the first trimester of a poorly controlled diabetic pregnancy. [Diabetologia (2001) 44: 209±219]

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“…Placenta is involved in nutrients transport and is considered an endocrine organ. Both insulin and IGF-1 receptors are abundant in placenta, mainly in trophoblastic tissue [14][15][16][17], which suggests that their ligands are regulators of amino acids and glucose transport needed for placental and fetal growth. Since preeclampsia is associated with intrauterine growth retardation, the objective of this study was to determine whether IR and IGF-1R ligand binding characteristics are altered in preeclamptic placentas.…”

Section: Introductionmentioning

confidence: 98%

Placental insulin and insulin-like growth factor I receptors in normal and preeclamptic pregnancies

Díaz

Cárdenas

Ariza

et al. 2005

Clinical Biochemistry

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Ultrastructural Localization of Insulin Receptors in Human Placenta

Abstract: The data suggest a spatiotemporal alteration in placental IR distribution during pregnancy, possibly reflecting a shift in control of placental growth and metabolism from mother to fetus.

Cited by 41 publications

References 20 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

Hyperglycaemia in vitro alters the proliferation and mitochondrial activity of the choriocarcinoma cell lines BeWo, JAR and JEG-3 as models for human first-trimester trophoblast

Placental insulin and insulin-like growth factor I receptors in normal and preeclamptic pregnancies

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