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Fetal intrauterine growth restriction (IUGR) is a frequently occurring and serious complication of pregnancy. Infants exposed to IUGR are at risk for numerous perinatal morbidities, including hypoglycemia in the neonatal period, as well as increased risk of later physical and/or mental impairments, cardiovascular disease and non-insulin-dependent diabetes mellitus. Fetal growth restriction most often results from uteroplacental dysfunction during the later stage of pregnancy. As glucose, which is the most abundant nutrient crossing the placenta, fulfills a large portion of the fetal energy requirements during gestational development, and since impaired placental glucose transport is thought to result in growth restriction, we investigated the effects of maternal 50% food restriction (FR50) during the last week of gestation on rat placental expression of glucose transporters, GLUT1, GLUT3 and GLUT4, and on plasma glucose content in both maternal and fetal compartments. Moreover, as maternal FR50 induces fetal overexposure to glucocorticoids and since these hormones are potent regulators of placental glucose transporter expression, we investigated whether putative alterations in placental GLUT expression correlate with changes in maternal and/or fetal corticosterone levels.At term (day 21 of pregnancy), plasma glucose content was significantly reduced (P<0·05) in mothers subjected to FR50, but was not affected in fetuses. Food restriction reduced maternal body weight (P<0·001) but did not affect placental weight. Plasma corticosterone concentration, at term, was increased (P<0·05) in FR50 mothers. Fetuses from FR50 mothers showed reduced body weight (P<0·001) but higher plasma corticosterone levels (P<0·05). Adrenalectomy (ADX) followed by corticosterone supplementation of the mother prevented the FR50-induced rise in maternal plasma corticosterone at term. Food restriction performed on either sham-ADX or ADX mothers induced a similar reduction in the body weight of the pups at term (P<0·01). Moreover, plasma corticosterone levels were increased in pups from sham-ADX FR50 mothers (P<0·01) and in pups from ADX control mothers (P<0·01). Western blot analysis of placental GLUT proteins showed that maternal FR50 decreased placental GLUT3 protein levels in all experimental groups at term (P<0·05 and P<0·01), but did not affect either GLUT1 or GLUT4 protein levels. Northern blot analysis of placental GLUT expression showed that both GLUT1 and GLUT3 mRNA were not affected by the maternal feeding regimen or surgery.We concluded that prolonged maternal malnutrition during late gestation decreases maternal plasma glucose content and placental GLUT3 glucose transporter expression, but does not obviously affect fetal plasma glucose concentration. Moreover, the present results are not compatible with a role of maternal corticosterone in the development of growth-restricted rat fetuses.

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ZnO powder samples sized from 500 to 3 μm are annealed in reducing and oxidizing atmosphere, thus creating geometrical lattice defects which in the paramagnetic case can be detected with ESR. Predominantly oxygen vacancies, oxygen at interstitial sites, and the coupling of these two kinds of defects correlated to the observed ESR‐lines at g1 = 1.955, g2 = 1.958, and g3 = 1.987 are discussed. The variation of the grain sizes allows to distinguish between the centres in the layer near the surface and the bulk centres; this is also possible by means of the photosensitivity of the ESR‐singnals. The paramagnetic centres of the surface layer can be excluded, as their lines are broadened by the paramagnetic oxygen in the air, if the pressure is greater than 1330 Pa (10 Torr), and therefore not detectable by ESR.

Trophoblast invasion and migration, but not proliferation, are enhanced by IL-15. Our results suggest a role for IL-15 in the modulation of MMP-1 secretion by JEG-3 cells. Furthermore, we speculate, that IL-15 might be related to the changes of cell adhesion molecule phenotype during the process of invasion.

The present study investigated the expression of glycogenin, the protein primer for glycogen synthesis, and the high affinity glucose transporter isoform GLUT3 as a further potential regulator of cellular glycogen metabolism, in first trimester and term human placenta using immunohistochemistry and Western blotting. At term, glycogenin was most abundant in the endothelium of fetal vessels. Trophoblast as well as basal decidual cells were moderately stained. The glycogenin distribution pattern in first trimester placentae resembled that at term, but reactivity was generally less intense. Extravillous trophoblast and villous cytotrophoblast were the major sites of GLUT3 expression. Endothelial cells were also strongly labelled with the GLUT3 antiserum. Western blotting identified both free and glucosylated glycogenin, as well as a 48 kDa band reacting with GLUT3 antiserum in placental villous tissue. Glycogenin immunoreactivity remained unaffected by amylolytic glycogen digestion, although preceding electron microscopical examination demonstrated the presence of glycogen. These data may indicate that placental glycogenin can be recycled from the immature glycogen or that it is located on the surface of the glycogen molecule. In conclusion, the co-expression of glycogenin with GLUT3 might enable glycogen-storing cells to exchange glucose quite effectively according to prevailing metabolic demands of glycogen synthesis or degradation.

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