The Placenta: Not Just a Conduit for Maternal Fuels

Hay, William W.

doi:10.2337/diab.40.2.s44

Cited by 42 publications

(39 citation statements)

References 45 publications

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“…The placenta is not only a passive transport vehicle or a mechanical barrier, it facilitates and regulates bidirectional transfer processes, modifies maternal nutrients destined for the fetus, and has its own active energy metabolism to support these activities (Sibley & Boyd 1988, Hay 1991. Efficient placental (maternal-to-fetal) transfer of glucose, the primary substrate for fetal oxidative metabolism, is crucial to sustain the normal development and survival of the fetus in utero, since it is not capable of producing appreciable amounts of glucose until late in gestation (Girard et al 1992).…”

Section: Introductionmentioning

confidence: 99%

Maternal undernutrition during late gestation-induced intrauterine growth restriction in the rat is associated with impaired placental GLUT3 expression, but does not correlate with endogenous corticosterone levels

Lésage¹,

Hahn²,

Léonhardt³

et al. 2002

Journal of Endocrinology

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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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Section: Introductionmentioning

confidence: 99%

Maternal undernutrition during late gestation-induced intrauterine growth restriction in the rat is associated with impaired placental GLUT3 expression, but does not correlate with endogenous corticosterone levels

Lésage¹,

Hahn²,

Léonhardt³

et al. 2002

Journal of Endocrinology

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“…The foetal liver contains approximately three times more glycogen than adult livers, and at birth this storage comprises < 1% of the neonate's energy reserves. Fat oxidation is thought to be quantitatively less important than amino acid/glucose oxidation during foetal life, and rates of ketone body production are low (Hay, 1991).…”

Section: Foetal Glycolysismentioning

confidence: 99%

Foetal and neonatal energy metabolism in pigs and humans: a review

Mota-Rojas¹,

Orozco-Gregorio²,

Villanueva-García³

et al. 2011

Vet. Med. - Czech

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ABSTRACT:The aim of this review was to elaborate a conceptual framework of the most important aspects of the main biochemical processes of synthesis and breakdown of energy substrates that human and pig foetuses and newborns can use during the transition from foetus to newborn. Under normal physiological conditions, the growth and development of the foetus depends upon nutrients such as glucose, lipids and amino acids. In addition to the maternal and foetal status, genetic factors are also reported to play a role. The main function of the placenta in all species is to promote the selective transport of nutrients and waste products between mother and foetus. This transport is facilitated by the close proximity of the maternal and foetal vascular systems in the placenta. The foetus depends on the placental supply of nutrients, which regulates energy reserves by means of glycogen storage. Also, the synthesis of foetal hepatic glycogen guarantees energy reserves during perinatal asphyxia or maternal hypoglycaemia. However, the foetus can also obtain energy from other resources, such as gluconeogenesis from the intermediary metabolism of the Krebs cycle and most amino acids. Later, when the placental glucose contribution ends during the transition to the postnatal period, the maturation of biological systems and essential metabolic adaptations for survival and growth is required. The maintenance of normoglycaemia depends on the conditions that determine nutrient status throughout life: the adequacy of glycogen stores, the maturation of the glycogenolytic and gluconeogenic pathway, and an integrated endocrine response.

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“…The fetal liver contains around three times more glycogen than adult liver, and at birth this storage comprises ϳ1% of the neonate's energy reserves. Fat oxidation is quantitatively thought to be less important than amino acid/glucose oxidation during fetal life, and rates of ketone body production are low (116).…”

Section: Glucose Homeostasis and Fetal Nutritionmentioning

confidence: 99%

Hyperinsulinism in Infancy: From Basic Science to Clinical Disease

Dunne

Cosgrove²,

Shepherd³

et al. 2004

Physiological Reviews

263

277

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Dunne, Mark J., Karen E. Cosgrove, Ruth M. Shepherd, Albert Aynsley-Green, and Keith J. Lindley. Hyperinsulinism in Infancy: From Basic Science to Clinical Disease. Physiol Rev 84: 239–275, 2004; 10.1152/physrev.00022.2003.—Ion channelopathies have now been described in many well-characterized cell types including neurons, myocytes, epithelial cells, and endocrine cells. However, in only a few cases has the relationship between altered ion channel function, cell biology, and clinical disease been defined. Hyperinsulinism in infancy (HI) is a rare, potentially lethal condition of the newborn and early childhood. The causes of HI are varied and numerous, but in almost all cases they share a common target protein, the ATP-sensitive K+ channel. From gene defects in ion channel subunits to defects in β-cell metabolism and anaplerosis, this review describes the relationship between pathogenesis and clinical medicine. Until recently, HI was generally considered an orphan disease, but as parallel defects in ion channels, enzymes, and metabolic pathways also give rise to diabetes and impaired insulin release, the HI paradigm has wider implications for more common disorders of the endocrine pancreas and the molecular physiology of ion transport.

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The Placenta: Not Just a Conduit for Maternal Fuels

Cited by 42 publications

References 45 publications

Maternal undernutrition during late gestation-induced intrauterine growth restriction in the rat is associated with impaired placental GLUT3 expression, but does not correlate with endogenous corticosterone levels

Maternal undernutrition during late gestation-induced intrauterine growth restriction in the rat is associated with impaired placental GLUT3 expression, but does not correlate with endogenous corticosterone levels

Foetal and neonatal energy metabolism in pigs and humans: a review

Hyperinsulinism in Infancy: From Basic Science to Clinical Disease

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