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  • 1
    Online Resource
    Online Resource
    Wiley ; 1985
    In:  Journal of Cellular Physiology Vol. 124, No. 3 ( 1985-09), p. 446-450
    In: Journal of Cellular Physiology, Wiley, Vol. 124, No. 3 ( 1985-09), p. 446-450
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 1985
    detail.hit.zdb_id: 1478143-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Cell Physiology Vol. 295, No. 5 ( 2008-11), p. C1445-C1453
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 295, No. 5 ( 2008-11), p. C1445-C1453
    Abstract: BeWo cells are a placental cell line that has been widely used as an in vitro model for the placenta. The b30 subclone of these cells can be grown on permeable membranes in bicameral chambers to form confluent cell layers, enabling rates of both nutrient uptake into the cells from the apical surface and efflux from the basolateral membrane to be determined. The aim of this study was to evaluate structural and functional properties of confluent b30 BeWo cell layers grown in bicameral chambers, focusing on the potential application for studying receptor-mediated uptake and transport of transferrin (Tf)-bound iron (Fe-Tf). While it proved extremely difficult to establish and maintain an intact BeWo cell monolayer, it was possible to grow the cells to a confluent multilayer. Iron, applied as Fe-Tf, was rapidly transported across this cell layer; 9.3 ± 0.5% of the total dose was transported after 8 h, equivalent to 38.8 ± 2.1 pmol·cm −2 ·h −1 . Transfer of Tf across the cell layer was much more limited; 2.4 ± 0.2% of the total dose was transported after 8 h, equivalent to 5.0 ± 0.4 pmol·cm −2 ·h −1 . Compartmental modeling of these data suggested that iron was transported across the cell layer predominantly, if not exclusively, via a transcellular route, whereas Tf taken up into the cells was predominantly recycled back to the apical compartment. The results suggest that these cells are very efficient at transporting iron and, under carefully controlled conditions, can be a valuable tool for the study of iron transport in the placenta.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 3
    In: Reproduction, Bioscientifica, Vol. 133, No. 3 ( 2007-03), p. 653-661
    Abstract: Glucocorticoids play a critical role in fetal development, but inappropriate exposure is associated with reduced fetal growth. We investigated cortisol exposure and supply in a porcine model of differential fetal growth. This model compares the smallest fetus of a litter with an average-sized sibling at three stages of gestation. At day 45, small fetuses had reduced plasma cortisol (16.8 ± 3.4 ng/ml) relative to average fetuses (34.4 ± 3.4 ng/ml, P 〈 0.001). At day 65 levels had reduced in small and average fetuses to similar concentrations (5.7 ± 1.0 vs 4.8 ± 0.5 ng/ml, P = 0.128). By day 100, elevated levels were found in small fetuses (10.7 ± 1.5 vs 7.6 ± 0.7 ng/ml, P 〈 0.001). Maternal plasma cortisol was unchanged over gestation (day 45, 56.7 ± 21.6 ng/ml; day 65, 57.8 ± 14.4 ng/ml; day 100, 55.7 ± 6.5 ng/ml). We examined the cause of altered cortisol by investigating the fetal hypothalamic–pituitary–adrenal axis through the measurement of adrenocorticotropic hormone and assessing exposure to maternal cortisol by quantifying placental 11β-hydroxysteroid dehydrogenase-isoform 2 ( 11 β HSD-2 ) gene expression. These data suggest that altered cortisol supply was of fetal origin. We examined organ glucocorticoid (GC) metabolism by the measurement of GC receptor (GR) and 11β-hydroxysteroid dehydrogenase-isoform 1 ( 11 β HSD-1 ) gene expression. We found that fetal organs have different temporal patterns of 11β HSD-1 and GR expression, with the liver particularly sensitive to cortisol in late gestation. This study examines GC exposure in naturally occurring differential growth and simultaneously explores tissue GC sensitivity and handling, at three key stages of gestation.
    Type of Medium: Online Resource
    ISSN: 1470-1626 , 1741-7899
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2007
    detail.hit.zdb_id: 2037813-0
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  • 4
    In: Journal of Toxicology and Environmental Health, Part B, Informa UK Limited, Vol. 13, No. 6 ( 2010-08-18), p. 449-459
    Type of Medium: Online Resource
    ISSN: 1093-7404 , 1521-6950
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2010
    detail.hit.zdb_id: 2011171-X
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  • 5
    In: Reproduction, Bioscientifica, Vol. 129, No. 6 ( 2005-06), p. 757-763
    Abstract: The fetus requires an adequate supply of fatty acids for optimum growth and development. It has been hypothesized that reduced activity of enzymes of fatty acid metabolism could contribute to inadequate fetal growth. In a porcine model of differential fetal growth we examined heart and liver fatty acid synthase, Δ5-desaturase and Δ6-desaturase gene expression and measured hepatic fatty acid profile to assess long-chain polyunsaturated fatty acid status. On gestation days 45, 65 and 100 sows were killed and tissues extracted from an average-sized fetus and the smallest fetus from each litter. As early as day 45, considerable hepatic Δ5- and Δ6-desaturase was detected, and this expression significantly increased as gestation progressed. In contrast, cardiac desaturase expression remained stable with time. Fatty acid synthase expression was greatest at day 65 in the liver, but was not expressed in the heart. Overall, the smallest fetus did not exhibit reduced tissue Δ5- or Δ6-desaturase expression or compromised polyunsaturated fatty acid status at any stage. In fact, small fetuses expressed more cardiac Δ5-desaturase than their average-sized siblings, possibly in response to a stress to the heart. It is clear from this study that fatty acid metabolism changes markedly as gestation progresses, and reduced fatty acid supply does not cause inadequate growth in this porcine model of fetal development.
    Type of Medium: Online Resource
    ISSN: 1470-1626 , 1741-7899
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2005
    detail.hit.zdb_id: 2037813-0
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  • 6
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 121, No. 2 ( 2019-01-28), p. 121-129
    Abstract: Fe deficiency is relatively common in pregnancy and has both short- and long-term consequences. However, little is known about the effect on the metabolism of other micronutrients. A total of fifty-four female rats were fed control (50 mg Fe/kg) or Fe-deficient diets (7·5 mg/kg) before and during pregnancy. Maternal liver, placenta and fetal liver were collected at day 21 of pregnancy for Cu and Zn analysis and to measure expression of the major genes of Cu and Zn metabolism. Cu levels increased in the maternal liver ( P =0·002) and placenta ( P =0·018) of Fe-deficient rats. Zn increased ( P 〈 0·0001) and Cu decreased ( P =0·006) in the fetal liver. Hepatic expression of the Cu chaperones antioxidant 1 Cu chaperone ( P =0·042) and cytochrome c oxidase Cu chaperone ( COX17 , P =0·020) decreased in the Fe-deficient dams, while the expression of the genes of Zn metabolism was unaltered. In the placenta, Fe deficiency reduced the expression of the chaperone for superoxide dismutase 1, Cu chaperone for superoxide dismutase ( P =0·030), ceruloplasmin ( P =0·042) and Zn transport genes, ZRT/IRT-like protein 4 ( ZIP4 , P =0·047) and Zn transporter 1 ( ZnT1, P =0·012). In fetal liver, Fe deficiency increased COX17 ( P =0·020), ZRT/IRT-like protein 14 ( P =0·036) and ZnT1 ( P =0·0003) and decreased ZIP4 ( P =0·004). The results demonstrate that Fe deficiency during pregnancy has opposite effects on Cu and Zn levels in the fetal liver. This may, in turn, alter metabolism of these nutrients, with consequences for development in the fetus and the neonate.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2016047-1
    SSG: 12
    SSG: 21
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  • 7
    In: Frontiers in Nutrition, Frontiers Media SA, Vol. 8 ( 2022-1-18)
    Abstract: A new variety of zinc biofortified wheat (Zincol-2016) was released in Pakistan in 2016. The primary aim of this study was to examine the effects of consuming Zincol-2016 wheat flour on biochemical and functional markers of zinc status in a population with widespread zinc deficiency. An individually-randomised, double-blind, placebo-controlled cross over design was used. Fifty households were recruited to participate in the study, with each household included at least one woman of reproductive age (16–49 years) who was neither pregnant nor breast feeding or currently taking nutritional supplements. All households were provided with control flour for an initial 2-week baseline period, followed by the intervention period where households were randomly allocated in a 1:1 ratio to receive biofortified flour (group A; n = 25) and control flour (group B; n = 25) for 8-weeks, then switched to the alternate flour for 8-weeks. The trial has been registered with the ISRCTN ( https://www.isrctn.com ), ID ISRCTN83678069. The primary outcome measure was plasma zinc concentration, and the secondary outcome measures were plasma selenium and copper concentrations, plasma copper:zinc ratio and fatty acid desaturase and elongase activity indices. Nutrient intake was assessed using 24-h dietary recall interviews. Mineral concentrations in plasma were measured using inductively coupled plasma mass spectrometry and free fatty acids and sphingolipids by mass spectrometry. Linear Mixed Model regression and General Linear Model with repeated measures were used to analyse the outcomes. Based on an average flour consumption of 224 g/day, Zincol-2016 flour provided an additional daily zinc intake of between 3.0 and 6.0 mg for white and whole grain flour, respectively. No serious adverse events were reported. This resulted in significant, increase in plasma zinc concentration after 4 weeks [mean difference 41.5 μg/L, 95% CI (6.9–76.1), p = 0.02]. This was not present after 8 weeks ( p = 0.6). There were no consistent significant effects of the intervention on fatty acid desaturase and elongase activity indices. Regular consumption of Zincol-2016 flour increased the daily zinc intake of women of reproductive age by 30–60%, however this was not associated with a sustained improvement in indices of zinc status.
    Type of Medium: Online Resource
    ISSN: 2296-861X
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2776676-7
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  • 8
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2018-06-13)
    Abstract: Iron overload due to environmental or genetic causes have been associated diabetes. We hypothesized that prenatal iron exposure is associated with higher risk of childhood type 1 diabetes. In the Norwegian Mother and Child cohort study (n = 94,209 pregnancies, n = 373 developed type 1 diabetes) the incidence of type 1 diabetes was higher in children exposed to maternal iron supplementation than unexposed (36.8/100,000/year compared to 28.6/100,000/year, adjusted hazard ratio 1.33, 95%CI: 1.06–1.67). Cord plasma biomarkers of high iron status were non-significantly associated with higher risk of type 1 diabetes (ferritin OR = 1.05 [95%CI: 0.99–1.13] per 50 mg/L increase; soluble transferrin receptor: OR = 0.91 [95%CI: 0.81–1.01] per 0.5 mg/L increase). Maternal but not fetal HFE genotypes causing high/intermediate iron stores were associated with offspring diabetes (odds ratio: 1.45, 95%CI: 1.04, 2.02). Maternal anaemia or non-iron dietary supplements did not significantly predict type 1 diabetes. Perinatal iron exposures were not associated with cord blood DNA genome-wide methylation, but fetal HFE genotype was associated with differential fetal methylation near HFE . Maternal cytokines in mid-pregnancy of the pro-inflammatory M1 pathway differed by maternal iron supplements and HFE genotype. Our results suggest that exposure to iron during pregnancy may be a risk factor for type 1 diabetes in the offspring.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2615211-3
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  • 9
    Online Resource
    Online Resource
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 291, No. 3 ( 2006-09), p. E596-E603
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 291, No. 3 ( 2006-09), p. E596-E603
    Abstract: Both placental system A activity and fetal plasma cortisol concentrations are associated with intrauterine growth retardation, but it is not known if these factors are mechanistically related. Previous functional studies using hepatoma cells and fibroblasts produced conflicting results regarding the regulation of system A by cortisol. Using the b30 BeWo choriocarcinoma cell line, we investigated the regulation of system A by cortisol. System A function was analyzed using methyl amino isobutyric acid (MeAIB) transcellular transport studies. Transporter expression [system A transporter (SNAT)1/2] was studied at the mRNA and protein levels using Northern and Western blotting, respectively. Localization was carried out using immunocytochemistry. The [ 14 C]MeAIB transfer rate across BeWo monolayers after preincubation with cortisol for 24 h was significantly increased compared with control. This was associated with a relocalization of the SNAT2 transporter at lower cortisol levels and significant upregulation of mRNA and protein expression levels at cortisol levels 〉 1 μM. This is the first study to show functional and molecular regulation of system A by cortisol in BeWo cells. It is also the first study to identify which system A isoform is regulated. These results suggest that cortisol may be involved in upregulation of system A in the placenta to ensure sufficient amino acid supply to the developing fetus.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Bioscientifica ; 2004
    In:  Reproduction Vol. 128, No. 2 ( 2004-08), p. 229-235
    In: Reproduction, Bioscientifica, Vol. 128, No. 2 ( 2004-08), p. 229-235
    Abstract: Low birth weight is a major factor in neonatal morbidity and mortality in humans and domestic species and is a predictor of physiological disorders in adulthood. This study utilised the naturally occurring variation in pig fetal size within a uterus to test the hypothesis that placental amino acid transport capability is associated with fetal growth. Leucine uptake by trophoblast vesicles prepared from placentas supplying an average-sized fetus and the smallest fetus in the uterus was assessed. On days 45 and 65 of gestation, uptake of leucine by the porcine placenta was predominantly sodium independent and was inhibited by the non-metabolised leucine analogue 2-amino-2-norbornane-carboxylic acid, indicating that uptake occurs via system L. By day 100 the uptake of leucine by placentas supplying average-sized fetuses had changed from being predominantly sodium independent to involving both sodium-dependent (system B 0 ) and -independent (system L) pathways. This change was not seen in placentas supplying the smallest fetus, which continued to display predominantly sodium-independent uptake. In conclusion, these data show gestational- and fetal size-dependent changes in the transport of leucine across the porcine placenta.
    Type of Medium: Online Resource
    ISSN: 1470-1626 , 1741-7899
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2004
    detail.hit.zdb_id: 2037813-0
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