Intrauterine growth restriction modifies the hedonic response to sweet taste in newborn pups – Role of the accumbal μ-opioid receptors

Neuroscience ◽  
2016 ◽  
Vol 322 ◽  
pp. 500-508 ◽  
Author(s):  
D.P. Laureano ◽  
R. Dalle Molle ◽  
M.B. Alves ◽  
C. Luft ◽  
M. Desai ◽  
...  
Keyword(s):  
Opioid Receptors ◽  
Intrauterine Growth Restriction ◽  
Sweet Taste ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Μ Opioid Receptors

scholarly journals Intrauterine Growth Restriction and the Fetal Programming of the Hedonic Response to Sweet Taste in Newborn Infants

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Caroline Ayres ◽  
Marilyn Agranonik ◽  
André Krumel Portella ◽  
Françoise Filion ◽  
Celeste C. Johnston ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Fetal Programming ◽  
Intrauterine Growth Restriction ◽  
Sucrose Solution ◽  
Sweet Taste ◽  
Growth Restriction ◽  
Fetal Life ◽  
Intrauterine Growth ◽  
Sweet Solution ◽  
Increased Risk

Intrauterine growth restriction is associated with increased risk for adult metabolic syndrome and cardiovascular disease, which seems to be related to altered food preferences in these individuals later in life. In this study, we sought to understand whether intrauterine growth leads to fetal programming of the hedonic responses to sweet. Sixteen 1-day-old preterm infants received 24% sucrose solution or water and the taste reactivity was filmed and analyzed. Spearman correlation demonstrated a positive correlation between fetal growth and the hedonic response to the sweet solution in the first 15 seconds after the offer (r=0.864,P=0.001), without correlation when the solution given is water (r=0.314,P=0.455). In fact, the more intense the intrauterine growth restriction, the lower the frequency of the hedonic response observed. IUGR is strongly correlated with the hedonic response to a sweet solution in the first day of life in preterm infants. This is the first evidence in humans to demonstrate that the hedonic response to sweet taste is programmed very early during the fetal life by the degree of intrauterine growth. The altered hedonic response at birth and subsequent differential food preference may contribute to the increased risk of obesity and related disorders in adulthood in intrauterine growth-restricted individuals.

The Role of the Anti-Angiogenic Factor Endostatin in Intrauterine Growth Restriction

2005 ◽  
Vol 12 (3) ◽  
pp. 195-197 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Evangelos Makrakis ◽  
Zoe Iliodromiti ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Angiogenic Factor ◽  
Intrauterine Growth

The brain development of infants with intrauterine growth restriction: role of glucocorticoids

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Ying-xue Ding ◽  
Hong Cui
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Intrauterine Growth Restriction ◽  
Growth And Development ◽  
Growth Restriction ◽  
Microvascular Endothelial Cells ◽  
Intrauterine Growth ◽  
Growth Restrictions ◽  
The Brain

Abstract Brain injury is a serious complication of intrauterine growth restriction (IUGR), but the exact mechanism remains unclear. While glucocorticoids (GCs) play an important role in intrauterine growth and development, GCs also have a damaging effect on microvascular endothelial cells. Moreover, intrauterine adverse environments lead to fetal growth restriction and the hypothalamus-pituitary-adrenal (HPA) axis resetting. In addition, chronic stress can cause a decrease in the number and volume of astrocytes in the hippocampus and glial cells play an important role in neuronal differentiation. Therefore, it is speculated that the effect of GCs on cerebral neurovascular units under chronic intrauterine stimulation is an important mechanism leading to brain injury in infants with growth restrictions.

Angiopoietin-2 in the perinatal period and the role of intrauterine growth restriction

2006 ◽  
Vol 85 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Anastasia Tzonou ◽  
Evangelos Makrakis ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Perinatal Period ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Angiopoietin 2

scholarly journals The detrimental role of angiotensin receptor agonistic autoantibodies in intrauterine growth restriction seen in preeclampsia

2009 ◽  
Vol 206 (12) ◽  
pp. 2809-2822 ◽  
Author(s):  
Roxanna A. Irani ◽  
Yujin Zhang ◽  
Sean C. Blackwell ◽  
Cissy Chenyi Zhou ◽  
Susan M. Ramin ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Causative Factor ◽  
Growth Restriction ◽  
Hypertensive Disorder ◽  
Human Trophoblast ◽  
Fetal Circulation ◽  
Intrauterine Growth ◽  
Underlying Mechanisms ◽  
Agonistic Autoantibodies

Growth-restricted fetuses are at risk for a variety of lifelong medical conditions. Preeclampsia, a life-threatening hypertensive disorder of pregnancy, is associated with fetuses who suffer from intrauterine growth restriction (IUGR). Recently, emerging evidence indicates that preeclamptic women harbor AT1 receptor agonistic autoantibodies (AT1-AAs) that contribute to the disease features. However, the exact role of AT1-AAs in IUGR and the underlying mechanisms have not been identified. We report that these autoantibodies are present in the cord blood of women with preeclampsia and retain the ability to activate AT1 receptors. Using an autoantibody-induced animal model of preeclampsia, we show that AT1-AAs cross the mouse placenta, enter fetal circulation, and lead to small fetuses with organ growth retardation. AT1-AAs also induce apoptosis in the placentas of pregnant mice, human villous explants, and human trophoblast cells. Finally, autoantibody-induced IUGR and placental apoptosis are diminished by either losartan or an autoantibody-neutralizing peptide. Thus, these studies identify AT1-AA as a novel causative factor of preeclampsia-associated IUGR and offer two possible underlying mechanisms: a direct detrimental effect on fetal development by crossing the placenta and entering fetal circulation, and indirectly through AT1-AA–induced placental damage. Our findings highlight AT1-AAs as important therapeutic targets.

The role of methylentetrahydrofolate reductase (MTHFR) gene polymorphism in intrauterine growth restriction development

2018 ◽  
Vol 12_2018 ◽  
pp. 23-28
Author(s):  
Tyutyunnik V.L. Tyutyunnik ◽  
Kan N.E. Kan ◽  
Mantrova D.A. Mantrova ◽  
Lomova N.A. Lomova N ◽  
Klimantsev I.V. Klimantsev ◽  
...  
Keyword(s):  
Gene Polymorphism ◽  
Intrauterine Growth Restriction ◽  
Mthfr Gene ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Mthfr Gene Polymorphism ◽  
Methylentetrahydrofolate Reductase

The role of E-kadherin in the formation of intrauterine growth restriction

2018 ◽  
Vol 6_2018 ◽  
pp. 38-44
Author(s):  
Krasnyi A.M. Krasnyi ◽  
Khachaturyan A.A. Khachaturyan ◽  
Kan N.E. Kan ◽  
Khachatryan Z.V. Khachatryan Z ◽  
Tyutyunnik V.L. Tyutyunnik ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth

The role of proteome imbalance in the pathogenesis of intrauterine growth restriction

2020 ◽  
Vol 19 (3) ◽  
pp. 52-56
Author(s):  
T.N. Pogorelova ◽  
◽  
V.O. Gunko ◽  
N.V. Palieva ◽  
I.G. Pelipenko ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth

The role of regulatory autoantibodies in predicting a risk for intrauterine growth restriction

2016 ◽  
Vol 15 (1) ◽  
pp. 30-34
Author(s):  
R.S. Zamaleeva ◽  
◽  
V.K. Lazareva ◽  
N.A. Cherepanova ◽  
M.E. Zhelezova ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth
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