Hyperglycaemia-induced subcellular redistribution of GLUT1 glucose transporters in cultured human term placental trophoblast cells

Hahn, Tom; Hahn, Dietger; Blaschitz, Astrid; Korgun, Emin Türkay; Desoyé, Gernot; Dohr, Gottfried

doi:10.1007/s001250050026

Cited by 58 publications

(27 citation statements)

References 52 publications

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“…One possibility for the decrease in the uptake we have observed in this study is that the deficit of insulin in the STZ-treated animals resulted in a decrease in the number of uptake sites due either to a decrease in the synthesis of carrier protein or to translocation of the carriers to intracellular stores. Another possibility is that the increased glucose concentrations in diabetic animals may result in subcellular redistribution of amino acid uptake sites in tubular epithelial cells as has been described for glucose transporters in the kidney [25, 26]and other tissues [27]. In agreement with this hypothesis is the reported finding of increased urinary excretion of aromatic amino acids in nonketotic diabetic dogs [28].…”

Section: Discussionsupporting

confidence: 78%

Decreased Tubular Uptake of <i>L</i>-3,4-Dihydroxyphenylalanine in Streptozotocin-Induced Diabetic Rats

Carranza¹,

Karabatas²,

Barontini³

et al. 2001

Horm Res Paediatr

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Background/Aims: This study determined alterations in renal dopamine production in streptozotocin-treated rats and explored the mechanisms underlying this alteration. Methods: Streptozotocin (65 mg/kg) or vehicle was administered to 3-month-old male Wistar rats. Treated animals had hyperglycemia, glycosuria and increased diuresis, natriuresis and excretion of L-dopa. Urinary dopamine and dihydroxyphenylacetic acid were similar to those in control animals. The production of dopamine by renal cortex slices from treated rats was significantly less than that from control animals. The addition of glucose (8.4–18.4 mM) to the incubation medium decreased about 40% the uptake of L-dopa by isolated proximal tubular cells. Scatchard analysis of the saturation curves obtained in this condition showed a decrease in the V_max without changes in the K_m. Results: Our results confirm previous studies suggesting a renal dopaminergic deficiency in insulin-dependent diabetes and provide evidence strongly suggesting that a decrease in the number of tubular L-dopa transport sites is the underlying defect of this deficiency. Conclusion: These results highlight the role of the uptake of dopa as an important modulator of renal dopamine synthesis.

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Section: Discussionsupporting

confidence: 78%

Decreased Tubular Uptake of <i>L</i>-3,4-Dihydroxyphenylalanine in Streptozotocin-Induced Diabetic Rats

Carranza¹,

Karabatas²,

Barontini³

et al. 2001

Horm Res Paediatr

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“…Hyperglycaemia has been shown to reduce cultured human term trophoblast cell glucose uptake through a reduction in GLUT1 protein expression and translocation of GLUT1 away from the cell surface [15,16]. The glycated haemoglobin measurements in this study suggest that long-term glycaemic control was not different between the two GDM groups.…”

Section: Discussionmentioning

confidence: 46%

“…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%

“…This procedure was repeated until samples had been collected for each of the 4, 8, 16 or 24 mmol/l maternal glucose concentrations for each placenta. The perfusion of each maternal glucose concentration took 51 min and the entire experiment was completed within 4.5 h. The samples collected for the 4,8,16 or 24 mmol/l maternal glucose concentrations were centrifuged immediately at 3000 rpm for 5 min to remove any trace of blood and assayed fresh for glucose and llactate using a YSI 2300 analyser (YSI, Yellow Springs, Ohio, USA). is the fetal effluent glucose concentration(mmol/ml); V M is the maternal perfusion rate (ml/min); V F is the fetal perfusion rate (ml/min); W is the perfused lobule weight (grams wet weight); G C14 FE is the 14 C-d-glucose activity in the fetal effluent (dpm/mmol); G C14 MP is the 14 C-d-glucose activity in the maternal perfusate (dpm/mmol); L ME is the lactate concentration in the maternal effluent (mmol/ml); L FE is the lactate concentration in the fetal effluent (mmol/ml).…”

Section: Methodsmentioning

confidence: 99%

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

et al. 2001

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“…The ubiquitously expressed GLUT-1 isoform is inversely related to extracellular glucose concentration in placenta (17) whereas GLUT-4, which is found to a lesser extent in the placenta, are insulin sensitive GLUTs (18). Studies have demonstrated diminished glucose uptake in placental tissue from individuals with GDM (19)(20)(21)(22) and furthermore, increased expression of GLUT-1 in placenta basal membranes from GDM women in comparison with normal controls (23,24).…”

Section: Introductionmentioning

confidence: 99%

Defective insulin signaling in placenta from pregnancies complicated by gestational diabetes mellitus

Colomiere¹,

Permezel²,

Riley³

et al. 2009

European Journal of Endocrinology

177

125

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Objective: Studies in adipose tissue and skeletal muscle suggest that impaired insulin action is due to defects in the insulin signaling pathway and may play a role in the pathophysiology of insulin resistance associated with gestational diabetes mellitus (GDM) and obesity. The present study tested the hypothesis that endogenous expression levels in the human term placenta of insulin signaling components are altered in placental tissue from GDM women in comparison with normal controls and maternal obesity. Design and methods: Placental tissue was collected from normal, diet-controlled GDM, and insulincontrolled GDM in both non-obese and obese women (nZ6-7 per group). Western blotting and quantitative RT-PCR was performed to determine the level of expression in the insulin signaling pathway.Results: There was a significant increase in insulin receptor (IR) substrate (IRS)-1 protein expression with a concurrent decrease in IRS-2 protein expression in non-obese women with insulin-controlled GDM compared with diet-controlled GDM and normal controls. Furthermore, a decrease in both protein and mRNA expression of phosphatidyl-inositol-3-kinase (PI3-K) p85a and glucose transporter (GLUT)-4 was observed in non-obese and obese women with insulin controlled GDM compared with normal controls. When comparing non-obese to obese patients, significant decreases in mRNA expression of IR-b, PI3K p85a and GLUT-4 was found in obese patients. Conclusion: Our results suggest that post receptor defects are present in the insulin signaling pathway in placenta of women with pregnancies complicated by diabetes and obesity. In addition, expression studies demonstrate post receptor alterations in insulin signaling possibly under selective maternal regulation and not fetal regulation.

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Hyperglycaemia-induced subcellular redistribution of GLUT1 glucose transporters in cultured human term placental trophoblast cells

Cited by 58 publications

References 52 publications

Decreased Tubular Uptake of <i>L</i>-3,4-Dihydroxyphenylalanine in Streptozotocin-Induced Diabetic Rats

Decreased Tubular Uptake of <i>L</i>-3,4-Dihydroxyphenylalanine in Streptozotocin-Induced Diabetic Rats

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

Defective insulin signaling in placenta from pregnancies complicated by gestational diabetes mellitus

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