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T Jansson

Publications and source records attributed to T Jansson.

At least 55 records · Page 3Linked to original sources

Chloride transport across syncytiotrophoblast microvillous membrane of first trimester human placenta.

There are significant changes in the activity of some placental transporters between first trimester and term. However, chloride transport has previously been studied only in the term placenta. Therefore. in this study, we investigated chloride transport mechanisms in syncytiotrophoblast microvillous membrane (MVM) vesicles from first trimester human placentas and compared them with those in vesicles from term placentas. 36Cl- uptake into MVM vesicles was linear up to 45 s and had reached equilibrium by 1 h for both first trimester and term vesicles. In first trimester MVM at 0 mV, 0.1 mM diisothiocyano-2,2'-disulfonic stilbene (DIDS) blocked 25+/-3% (n=8) of 36Cl- uptake at 30 s (initial rate), which was similar to the 30+/-7% (n=6) inhibition by DIDS in term MVM. In the presence of a 25 mV inside-positive electrical potential difference, induced by imposition of a K+ gradient after preincubation with 200 microM valinomycin, 0.5 mM diphenylamine-2-carboxylate (DPC) significantly blocked 30+/-4% of 36Cl- uptake at 30 s by first trimester MVM (p < 0.01); 18+/-5% (n=8) of total uptake was inhibited by DPC but not by DIDS. There was a similar 15+/-3% (n=6) component of 36Cl- uptake by term MVM, which was inhibited by DPC but not by DIDS. Using Western blotting, it was shown that the anion exchanger-1 protein was expressed in first trimester MVM in quantitatively similar amounts to that in term MVM. This study suggests that there is both an anion exchanger and a DPC-sensitive conductance in MVM of first trimester placenta with activity similar to that of term human placenta.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Intrauterine growth restriction is associated with a reduced activity of placental taurine transporters.

Taurine is an essential amino acid during fetal life and appears to be vital for the growth of the fetus and for the development of the CNS. In intrauterine growth restriction (IUGR), fetal plasma concentrations of taurine are reduced, and we tested the hypothesis that this is caused by altered placental transport of taurine. Syncytiotrophoblast microvillous membrane (MVM) and basal membrane (BM) vesicles were isolated from control (fetal weight, 3068+/-191 g; gestational age, 37.0+/-0.7 wk; n=13) and IUGR pregnancies (fetal weight, 1724+/-118 g; gestational age, 35.8+/-0.7 wk; n=11). Uptake of [3H]taurine (0.5 microM) was studied at 22 degrees C using rapid filtration techniques. Sodium stimulated taurine uptake 35-fold in MVM, confirming Na+-dependent transport in this membrane. A Na+-dependent taurine transport could also be demonstrated in BM; however, the activity was only 6% of that in MVM. Na+-independent transport activities were similar in MVM and BM. In IUGR, MVM Na+-dependent taurine transport was reduced by 34% (p < 0.05), whereas Na+-independent uptake was unaltered. In contrast to MVM, Na+-dependent taurine uptake in BM was unaffected by IUGR, whereas Na+-independent transport was decreased by 33% (p < 0.05). The highly polarized distribution of the Na+/taurine cotransporter to the MVM in conjunction with similar Na+-independent transport rates for taurine in MVM and BM provides the basis for net taurine flux from the mother to the fetus. These data suggest that the low plasma concentrations of taurine in IUGR fetuses are caused by a reduced activity of placental taurine transporters.

Biological Transport↗

Placental transport of leucine and lysine is reduced in intrauterine growth restriction.

Intrauterine growth restriction (IUGR) is characterized by a reduction in fetal plasma concentrations of a number of essential amino acids. Whether this is caused by impaired placental transport is unknown. We studied transport of leucine and lysine in syncytiotrophoblast microvillous (MVM) and basal membrane (BM) vesicles isolated from uncomplicated (control) and IUGR pregnancies. In addition, we investigated the possibility that leucine uptake is stimulated by an outwardly directed glycine gradient. Uptake of 3H-L-lysine (0.1 microM) and 3H-L-leucine (0.25 microM) was studied at 37 degrees C using rapid filtration techniques. In IUGR, mediated uptake of lysine was reduced by 44% (p < 0.05) in BM and uptake of leucine was lower in both MVM (-46%, p < 0.05) and BM (-38%, p < 0.05) compared with control vesicles. Intravesicular glycine (2 mM) increased the uptake of leucine by 98% in MVM (p < 0.05). These data suggest that the activity of placental transporters for cationic and neutral amino acids is reduced in IUGR. We speculate that a reduced glycine gradient in the placenta in IUGR, due to reduction in system A activity, will impair leucine transport to the fetus, providing an additional mechanism for reduced placental transport of leucine in IUGR.

Biological Transport↗

Cloning of two novel growth hormone transcripts expressed in human placenta.

Several isoforms of human GH (hGH) are produced by two related genes expressed in the pituitary (hGH-N) and in the placenta (hGH-V). These genes consist of five exons (denoted 1-5) separated by four introns (denoted A-D). In the present report, two new transcripts of the hGH-V gene are described. The coding region of the hGH-V gene was amplified by RT-PCR using placental complementary DNA as template. DNA sequencing of several clones revealed two novel transcripts. One had a 45-bp deletion caused by the use of an alternative splice acceptor site within exon 3, similar to that in the hGH-N gene, predicting a 20-kDa isoform of hGH-V. The other transcript was generated by the use of an alternative splice donor site causing a 4-bp deletion in the end of exon 4, predicting a 24-kDa protein with 219 amino acids, which we refer to as hGH-V3. The carboxy-terminal sequence of hGH-V3 differs from 22-kDa hGH-V and hGH-V2, the two previously reported transcripts of the hGH-V gene, and does not contain a predicted transmembrane domain as described for hGH-V2. Ligase chain reaction was then used to analyze the possible use of the same splicing pattern in transcripts derived from the other genes of the hGH-gene cluster. Alternatively spliced transcripts encoding the 20-kDa hGH isoform were detected from the hGH-N and hGH-V genes, but not from the human chorionic somatomammotropin-A/B genes. The alternative splicing generating hGH-V3 was only demonstrated in transcripts derived from the hGH-V gene. Using competitive RT-PCR, the expression of hGH-V3 was estimated to be 10% of the hGH-V messenger RNA in full-term normal placentas and in placentas from pathological pregnancies. The 20-kDa hGH-V was detected in two of four full-term normal placentas, whereas a weak signal was observed in one of the pathological placentas. We conclude that the hGH-V primary transcript undergoes alternative splicing pathways generating at least four different messenger RNAs, predicting the expression of different hGH isoforms, including two with a complete sequence divergence in the carboxy-terminus.

Alternative Splicing↗

Ultrasound Doppler vector tomography measurements of directional blood flow.

An experimental system has been developed to verify the possibility of detecting flow activity using a technique called ultrasound Doppler vector tomography. A tomography algorithm is used to reconstruct blood flow vector fields using data from computer-controlled ultrasound continuous-wave Doppler scanning equipment. The result is a picture in which the brightness variations represent the reconstructed values of the curl of the velocity field (inverted delta x v). Continuous ultrasound is transmitted into a region with flow activity and the Doppler-shifted signals are received. To obtain measurement data suited for fan beam tomography, the scanning is performed in a plane from points encircling the region. Reconstructions have been achieved using measurement data from two different flow phantoms. A comparison between the experimental results and simulations shows good conformity.

Blood Circulation↗

Differential expression of protein kinase C isoforms in the human placenta.

The extensive role played by protein kinase C (PKC) in signal transduction prompted this study of the expression and localization of PKC isoforms in human placental syncytiotrophoblast. Membranes prepared from these cells and samples of villous tissue were analysed by immunoblotting and immunocytochemistry using isoform-specific antibodies. PKC beta 2, gamma, epsilon and zeta were found to be present in both microvillous and basal membranes from term placenta. The alpha isoform was observed only on the basal membrane while the beta 1 isoform was confined to the microvillous membrane. The basal microvillous ratios for beta 2, gamma, epsilon and zeta ranged between 0.3 and 0.5, demonstrating a substantial asymmetry in plasma membrane localization. Immunocytochemistry supported the isoform identification and localization observed in the immunoblotting experiments. Moreover the cellular distribution showed that the majority of syncytical PKC was bound to the plasma membranes, in contrast to the other villous cell types. Immunoblotting experiments demonstrated significant increases in PKC beta 2 and epsilon on the microvillous membrane and PKC gamma and epsilon on the basal membrane between 16 and 40 of weeks gestation. This is the first detailed mapping of PKC isoform distribution in an epithelial cell type and demonstrates the potential for selectivity in signal transduction through phosphorylation of isoform specific and spatially-separated substrates.

Amino Acid Sequence↗

Axial wall convergence of full veneer crown preparations. Documented for dental students and general practitioners.

The convergence angle in 478 full crown preparations was assessed. Of these preparations, 351 had been performed by general practitioners and 127 by dental students. Groups of preparations performed on incisors, premolars, and molars were compared, as were preparations performed by dentists and students. Two different convergence angles were measured for each tooth, buccolingually and mesiodistally. The results showed a mean angle of 21 degrees. The mean values for premolars and molars differed significantly. When a comparison was made of preparations performed by students, a significant difference was found between premolars and molars. The same comparison for general practitioners showed a significant difference both for incisors compared with molars and for premolars compared with molars. A wide range was found for the convergence of the axial walls, especially for the preparations performed by general practitioners.

Clinical Competence↗

Overview on human breast cancer with focus on prognostic and predictive factors with special attention on the tumour suppressor gene p53.

A long list of potential prognostic markers has been analysed for breast cancer, some of them will be reviewed in this article. The lymph node status is still the best prognostic marker. The lymph node status combined with information on tumour size, receptor- and proliferation status of the tumour should be analysed as standard for all breast cancer patients. Prognostic information for breast cancer patients has also been described for the membrane protein c-erbB2, the protease cathepsin D, plasminogen activators and inhibitors, certain oncogenes and tumour suppressor genes. Some of these factors also give potential additional information on the response to different oncological therapies, and are better denoted predictive factors. In this overview we shortly describe the above mentioned prognostic factors with major focus on the tumour suppressor gene p53 and its prognostic value and potential predictive value.

Apoptosis↗

Cellular localization of glucose transporter messenger RNA in human placenta.

High levels of expression of the glucose transporter (GLUT) isoforms 1 and 3 have been demonstrated in the human placenta by Northern blotting. However, the cellular localization of placental GLUT mRNA has not been described. Furthermore, recent preliminary kinetic data indicate that GLUT 2 might be present in syncytiotrophoblast. Human placental tissue from preterm (16-22 weeks) and term pregnancies was collected for identification and localization of glucose transporter mRNA. Following paraffin embedding, sections were cut and in situ hybridization was performed with fluorescein-labelled cRNA. In addition, immunoblotting and immunocytochemistry were carried out using an anti-GLUT 2 antibody. GLUT 1 mRNA was highly expressed in syncytiotrophoblast cells at term. GLUT 1 expression was much less abundant in non-syncytial cells. In contrast, GLUT 3 mRNA was present in lower amounts and more evenly distributed between syncytial and other placental cells. GLUT 1 mRNA was also highly abundant in preterm syncytiotrophoblast. The cellular distributions of GLUT 1 and GLUT 3 mRNA in the preterm placentas were similar to those in term tissue. With regard to GLUT 1, these findings correlate well with cellular localization and gestational development of GLUT 1 protein. No GLUT 2 protein was detected. It is concluded that GLUT 1 is the main isoform involved in transplacental glucose transport in the human.

Female↗

Automated correction of linear deformation due to sectioning in serial micrographs.

This paper describes an objective and automatic method for detection and correction of sectioning deformations in digitized micrographs, as well as an evaluation of the method applied to light and electron microscopic images of semi-thin and ultra-thin serial sections from brain cortex. The detection is based on matching of image subregions and the deformation model is bi-linear, i.e. two first-order polynomials are used for modelling compression/expansion in perpendicular directions. The procedure is applicable to prealigned serial two-dimensional sections and is primarily aimed at three-dimensional reconstruction of tissue samples consisting of a large number of cells with random distribution and morphology.

Animals↗

p53 Status predicts survival in breast cancer patients treated with or without postoperative radiotherapy: a novel hypothesis based on clinical findings.

PURPOSE AND METHODS: Primary breast cancer tumors without axillary metastases from 206 consecutive patients in a population-based cohort were investigated with regard to the presence of an intact p53 gene using a cDNA-based sequencing method. Clinical follow-up data and outcome of node-negative patients without any adjuvant systemic therapy (n = 168) were related to locoregional radiotherapy and p53 status. RESULTS: Mutations in p53 occurred in 31 node-negative breast cancer patients who did not receive any systemic adjuvant treatment, but were treated with postoperative locoregional radiotherapy or nothing. Node-negative breast cancer patients with p53 mutations had significantly improved relapse-free survival (P = .0007), breast cancer-corrected survival (P = .01), and overall survival (P = .02) rates when treated with locoregional radiotherapy. In node-negative breast cancer patients with wild-type p53, there was no statistically significant difference in outcome between patients who received locoregional radiotherapy and those who did not. Cox proportional hazards models indicate that mutant p53 is associated with worse prognosis independent of response to radiotherapy and that response to radiotherapy is qualitatively different in tumors with p53 mutations compared with those with wild-type p53. CONCLUSION: Our clinical findings define a group of breast cancer patients in whom locoregional radiotherapy improves relapse-free, breast cancer-corrected, and overall survival. The outcome for irradiated node-negative breast cancer patients with p53 alterations indicates that irradiation can induce cell death even in the presence of p53 mutations.

Adult↗

Positron emission tomography studies in patients with locally advanced and/or metastatic breast cancer: a method for early therapy evaluation?

PURPOSE: To investigate if sequential positron emission tomographic (PET) scans with the glucose analog 18F-2-fluoro-2-deoxy-D-glucose (18FDG) and/or L-methyl-11C-methionine (11C-methionine) in patients with breast cancer could provide early information on the efficacy of polychemotherapy. PATIENTS AND METHODS: Sixteen patients with breast cancer (11 with locally advanced tumors, three with recurrent disease in the contralateral breast, two of them with distant and regional metastases, and two with distant metastases) underwent a baseline and two follow-up PET scans after the first and third/fourth polychemotherapy course. Tumor response was determined clinically/radiographically after three/four polychemotherapy courses. RESULTS: Five patients were investigated with 18FDG, seven with both 11C-methionine and 18FDG, and four with only 11C-methionine before polychemotherapy. 11C-methionine presented a more distinct visualization of primary/contralateral breast cancers in five of seven patients when compared with 18FDG. Twelve of 16 patients demonstrated a response using conventional methods after the third/fourth course of polychemotherapy. Eight of these 12 clinical responders had a significant decrease in tracer uptake at the first PET scan performed 6 to 13 days after the first polychemotherapy course, and these reductions were further augmented after the third/fourth course and corresponded to the conventional therapy evaluation (clinical examination, computed tomography [CT], ultrasonography, and mammography). CONCLUSION: Our data indicate that PET may be of clinical value in predicting response to chemotherapy in patients with locally advanced breast cancer and/or metastatic disease earlier than any other method used.

Antineoplastic Combined Chemotherapy Protocols↗

Screening for agents inhibiting the mutagenicity of extracts and constituents of tobacco products.

The aim of this study was to screen for potential agents affecting the mutagenicity of tobacco products. The influence of a number of compounds which have been suggested to be antimutagenic some of which are present in tobacco products, was investigated on the mutagenicity of a cigarette smoke condensate (CSC) and, in some cases, an extract of oral Swedish moist snuff (SNUS), using a screening procedure of the Ames Salmonella/microsome assay (STY). For some of the compounds the V79/hprt mutagenicity assay with benzo[a]pyrene metabolites as mutagens was used to obtain complementary and confirmatory information on mammalian cells. The antimutagens used included two selenium compounds, sodium selenite and ebselen; the flavonoids and polyphenols, ellagic acid, (+)-catechin hydrate, scopoletin, chlorogenic acid and rutin trihydrate; the porphyrin derivatives, bovine hemin, biliverdine dihydrochloride, chlorophyllin and a plant extract containing chlorophyll; the terpenoids, beta-carotene, retinol and a mixture of the two epimers (4R) and (4S) of (1S,2E,6R,7E,11E)-cembra-2,7,11-triene-4,6-diols (CBD); and cyclohexanol and ubiquinone. Screening of antimutagenic activities using the STY involves problems with toxicity. In several cases in this study mutagenicity was decreased below the control level without signs of toxicity in the background growth of bacteria. Since the survival of mutants and slight bacteriostatic effects on the background growth cannot be determined accurately in the STY, a reduction in mutagenicity may simply be due to toxicity. Only in cases where a dose-response curve declines to a level at or above the background and then levels off, can toxicity be excluded. An antimutagenic effect determined using this test system is therefore often not sufficient for classifying a compound as antimutagenic until these findings are confirmed in other test systems and, preferably, the mechanism behind this effect is clarified. The results obtained with the selenium compounds were considered to be inconclusive since the reduction in the mutation rate declined below the background level and might only reflect the toxic effects of these compounds. For ellagic acid an almost complete inhibition of the mutagenicity of CSC and SNUS in STY was indicated. This indication of antimutagenicity was confirmed in V79 cells using two metabolites of the CSC constituent benzo[a]pyrene, i.e., trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene and (+)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-oxy-7,8,9,10- tetrahydrobenzo[a]pyrene (BPDE). Chlorogenic acid and (+)--catechin reduced the mutagenicity of CSC and chlorogenic acid also strongly inhibited SNUS mutagenicity. Scopoletin and rutin trihydrate inhibited the mutagenicity of CSC, but showed confounding effects with SNUS.(ABSTRACT TRUNCATED AT 400 WORDS)

Antimutagenic Agents↗

The cytotoxicity of 50 chemicals from the MEIC study determined by growth inhibition of ascites sarcoma BP8 cells: a comparison with acute toxicity data in man and rodents.

In this study, 50 chemicals selected on the basis of existence of particularly reliable human toxicity data were screened in a cytotoxicity test involving inhibition of the growth of Ascites Sarcoma BP8 cells. These test results are part of an international validation program, the Multicenter Evaluation of In Vitro Cytotoxicity (MEIC), the aim of which is to recommend batteries of in vitro tests to be used for prediction of human toxicity. The cytotoxicities (expressed as the concentrations causing 50% inhibition of cell growth) were compared to acute toxicity data in humans (LDL0) and rodents (LD50), showing the best correlation to rodent data. The results are discussed in relationship to what is usually referred to as basal cytotoxic mechanisms as a cause of in vivo toxicity. It could be concluded that the predicted results on the basis of mechanistic reasoning were not always obtained.

Animals↗

Possible improvement in uteroplacental blood flow during atrial natriuretic peptide infusion in preeclampsia.

OBJECTIVE: To study the effects of low doses of the hormone atrial natriuretic peptide (ANP) on uteroplacental blood flow in patients with preeclampsia. METHODS: Eleven women with preeclampsia were infused intravenously with ANP (10 ng/kg/minute). Uteroplacental blood flow index was measured using dynamic placental scintigraphy with indium-113m. Regional blood flows were assessed by pulsed Doppler ultrasound and expressed as pulsatility index (PI). Hemodynamic measurements and blood sampling for peripheral venous plasma analysis of cyclic guanosine monophosphate (cGMP), an ANP second messenger, were performed before and after 30 minutes of infusion. Nonparametric statistics were used. RESULTS: The uteroplacental blood flow index increased by 28% (-2 to 58%; mean and 95% confidence interval). The Doppler findings were unaffected. Mean arterial blood pressure decreased from 112 (108-117) to 108 (103-114) mmHg (P < .01). Cyclic GMP increased significantly from 9.2 (6.2-12.3) to 17.4 (12.3-22.6) nmol/L (P < .01). Subjects exhibiting a substantial increase in uteroplacental blood flow index (25% or more) demonstrated a significantly greater cGMP response (P < .01) than those who did not (6% or less increase). CONCLUSION: A tendency to an increased uteroplacental blood flow index combined with minor blood pressure reduction after ANP infusion suggest the possibility of uteroplacental vasodilatation.

Adult↗

Osmotic water permeabilities of human placental microvillous and basal membranes.

Literature data suggest that water accumulation by the human fetus is driven by osmotic gradients of small solutes. However, the existence of such gradients has not been supported by prior measurements. Attempts to estimate the size of the gradient necessary to drive net water movement have been seriously hampered by the lack of permeability data for the syncytiotrophoblast membranes. Stopped-flow light scattering techniques were employed to measure the osmotic water permeability (Pf) of microvillous (MVM) and basal membrane (BM) vesicles isolated from human term placenta. At 37 degrees C, the Pf was determined to be 1.9 +/- 0.06 x 10(-3) cm/sec for MVM and 3.1 +/- 0.20 x 10(-3) cm/sec for BM (mean +/- SD, n = 6). At 23 degrees C, Pf was reduced to 0.7 +/- 0.04 x 10(-3) cm/sec in MVM and 1.6 +/- 0.05 x 10(-3) cm/sec in BM. These Pf values are comparable to those observed in membranes where water has been shown to permeate via a lipid diffusive mechanism. Arrhenius plots of Pf over the range 20-40 degrees C were linear, with activation energies of 13.6 +/- 0.6 kcal/mol for MVM and 12.9 +/- 1.0 kcal/mol for BM. Water permeation was not affected by mercurial sulfhydryl agents and glucose transport inhibitors. These data clearly suggest that water movement across human syncytiotrophoblast membranes occurs by a lipid diffusion pathway. As noted in several other epithelial tissues, the basal membrane has a higher water permeability than the microvillous membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Non-electrolyte solute permeabilities of human placental microvillous and basal membranes.

1. Permeability to non-electrolytes of isolated microvillous and basal membranes from human term placenta was measured using stopped-flow light-scattering techniques. The studied solutes were urea, ethylene glycol, glycerol, creatinine, erythritol, arabitol and mannitol. 2. At 37 degrees C, permeability of the microvillous membrane to mannitol and urea was 0.30 +/- 0.02 x 10(-6) cm/s (mean +/- S.E.M.) and 3.2 +/- 0.2 x 10(-6) cm/s, respectively. The corresponding permeabilities for the basal membrane were 1.2 +/- 0.1 x 10(-6) cm/s (mannitol) and 4.4 +/- 0.3 x 10(-6) cm/s (urea). The basal membrane was substantially more permeable to hydrophilic solutes than the microvillous membrane. This is probably due to differences in lipid composition, as illustrated by membrane cholesterol content, which was found to be approximately 50% lower in the basal as compared to the microvillous membrane. 3. Similarities between permeabilities in placental membranes and lipid bilayers and the linear relationship noted between solute hydrophobicity and placental permeability suggested that solutes permeate both human syncytiotrophoblast membranes by a solubility/diffusion mechanism. In the microvillous membrane this was supported by data obtained for activation energies (> 10 kcal/mol) and reflection coefficients (close to 1). In the basal membrane, low activation energies for glycerol and urea and a low reflection coefficient for urea indicated that these solutes may, in part, share a common pathway with water. 4. It was estimated that the placental permeability to molecules with a molecular weight under 200 observed in vivo can, to a great extent, be accounted for by transcellular permeation.

Cell Membrane↗

Glucose transporter protein expression in human placenta throughout gestation and in intrauterine growth retardation.

Despite the importance of glucose for fetal growth, gestational development of placental glucose transport capacity has not been studied in the human. Furthermore, inadequate glucose transport has been implicated as a pathophysiological mechanism in intrauterine growth retardation (IUGR). We studied glucose transporter (GLUT) protein expression in sections of normal term placental tissue (immunocytochemistry) and in syncytiotrophoblast microvillous (MVM) and basal membranes (BM) isolated from normal term, preterm, and IUGR placentas (immunoblotting). GLUT 1, but not GLUT 3, protein was abundantly present in syncytiotrophoblast membranes. MVM had approximately 3-fold higher GLUT 1 density than BM at term. MVM GLUT 1 density was maintained from 16 weeks of gestation to term. BM GLUT 1 density increased 2-fold in late second trimester and remained unaltered thereafter to term. GLUT 1 densities in term and preterm IUGR placentas were unaltered. Net D-glucose uptake rates corresponded to the GLUT 1 densities. These data suggest that 1) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast; 2) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM; 3) GLUT 1 densities may be regulated independently in MVM and BM; 4) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy; and 5) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density.

Adult↗