Fetal Alcohol Exposure and Functional Implications of the Neuroimmune-Endocrine Networks

2022 ◽  
pp. 113-144
Author(s):  
Zehava Gottesfeld
Keyword(s):  
Alcohol Exposure ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol ◽  
Functional Implications

scholarly journals Fetal Alcohol Exposure Disrupts Metabolic Signaling in Hypothalamic Proopiomelanocortin Neurons via a Circadian Mechanism in Male Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2578-2588 ◽  
Author(s):  
Maria A. Agapito ◽  
Changqing Zhang ◽  
Sengottuvelan Murugan ◽  
Dipak K. Sarkar
Keyword(s):  
Alcohol Exposure ◽  
Male Mice ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol ◽  
Metabolic Signaling

Prevalence of heavy fetal alcohol exposure by analysis of meconium fatty acid ethyl esters; A nat ionwide canadian study

2018 ◽  
Vol 80 ◽  
pp. 142
Author(s):  
Kaithlyn Delano ◽  
Gideon Koren ◽  
Martin Zack ◽  
Bhushan Kapur ◽  
Joey Gareri ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Alcohol Exposure ◽  
Fatty Acid Ethyl Esters ◽  
Ethyl Esters ◽  
Fetal Alcohol Exposure ◽  
Canadian Study ◽  
Fetal Alcohol

scholarly journals Fetal Alcohol Exposure Increases Mammary Tumor Susceptibility and Alters Tumor Phenotype in Rats

2010 ◽  
Vol 34 (11) ◽  
pp. 1879-1887 ◽  
Author(s):  
Tiffany A. Polanco ◽  
Catina Crismale-Gann ◽  
Kenneth R. Reuhl ◽  
Dipak K. Sarkar ◽  
Wendie S. Cohick
Keyword(s):  
Mammary Tumor ◽  
Alcohol Exposure ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol ◽  
Tumor Susceptibility ◽  
Tumor Phenotype

scholarly journals Fetal Alcohol Exposure: The Common Toll

2017 ◽  
Vol 05 (01) ◽  
Author(s):  
Marie R Nakhoul ◽  
Karl E Seif ◽  
Natasha Haddad ◽  
Georges E Haddad
Keyword(s):  
Alcohol Exposure ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol ◽  
The Common

Fetal Alcohol Exposure: Effects on the Developing Brain

NeoReviews ◽  
2001 ◽  
Vol 2 (10) ◽  
pp. 231e-237 ◽  
Author(s):  
C. A. Gleason
Keyword(s):  
Alcohol Exposure ◽  
Developing Brain ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol

scholarly journals Long-lasting alterations to DNA methylation and ncRNAs could underlie the effects of fetal alcohol exposure in mice

2013 ◽  
Vol 6 (4) ◽  
pp. 977-992 ◽  
Author(s):  
B. I. Laufer ◽  
K. Mantha ◽  
M. L. Kleiber ◽  
E. J. Diehl ◽  
S. M. F. Addison ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Alcohol Exposure ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol

Binge alcohol exposure in the second trimester attenuates fetal cerebral blood flow response to hypoxia

2007 ◽  
Vol 102 (3) ◽  
pp. 972-977 ◽  
Author(s):  
Dennis E. Mayock ◽  
Dana Ness ◽  
Robin L. Mondares ◽  
Christine A. Gleason
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Damage ◽  
Alcohol Exposure ◽  
Oxygen Metabolism ◽  
Developed Countries ◽  
Cerebrovascular Reactivity ◽  
Second Trimester ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol

Alcohol is detrimental to the developing brain and remains the leading cause of mental retardation in developed countries. The mechanism of alcohol brain damage remains elusive. Studies of neurological problems in adults have focused on alcohol's cerebrovascular effects, because alcoholism is a major risk factor for stroke and cerebrovascular injuries. However, few studies have examined similar cerebrovascular effects of fetal alcohol exposure. We examined the effect of chronic binge alcohol exposure during the second trimester on fetal cerebrovascular and metabolic responses to hypoxia in near-term sheep and tested the hypothesis that fetal alcohol exposure would attenuate cerebrovascular dilation to hypoxia. Pregnant ewes were infused with alcohol (1.5 g/kg) or saline intravenously at 60–90 days of gestation (full term = 150 days). At 125 days of gestation, we measured fetal cerebral blood flow (CBF) and oxygen metabolism at baseline and during hypoxia. Maternal blood alcohol averaged 214 ± 5.9 mg/dl immediately after the 1.5-h infusion, with similar values throughout the month of infusion. Hypoxia resulted in a robust increase in CBF in saline-infused fetuses. However, the CBF response to hypoxia in fetuses chronically exposed to alcohol was significantly attenuated. Cerebral oxygen delivery decreased in both groups of fetuses during hypoxia but to a greater degree in the alcohol-exposed fetuses. Prenatal alcohol exposure during the second trimester attenuates cerebrovascular responses to hypoxia in the third trimester. Altered cerebrovascular reactivity might be one mechanism for alcohol-related brain damage and might set the stage for further brain injury if a hypoxic insult occurs.

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