PMID- 19038697
OWN - NLM
STAT- MEDLINE
DCOM- 20090205
LR  - 20211020
IS  - 1873-6823 (Electronic)
IS  - 0741-8329 (Print)
IS  - 0741-8329 (Linking)
VI  - 42
IP  - 8
DP  - 2008 Dec
TI  - Chronic binge ethanol-mediated acidemia reduces availability of glutamine and 
      related amino acids in maternal plasma of pregnant sheep.
PG  - 657-66
LID - 10.1016/j.alcohol.2008.08.008 [doi]
AB  - Heavy drinking during pregnancy can result in fetal alcohol syndrome (FAS), of 
      which, fetal and postnatal growth retardation and central nervous system deficits 
      are cardinal features. Although a number of mechanisms have been proposed, none 
      fully account for these deficiencies. We have previously reported that maternal 
      ethanol exposure (1.75 g/kg) results in transient acidemia in the mother and 
      fetus. Alterations in pH are known to regulate glutamine homeostasis. Therefore, 
      we hypothesized that chronic binge ethanol-mediated acidosis reduces glutamine 
      concentrations in maternal plasma that result in decreases in the circulating 
      levels of amino acids related to glutamine metabolism. Pregnant ewes were divided 
      into three groups: ethanol (1.75 g/kg), saline control, and acidemia (inspired 
      fractional carbon dioxide [CO(2)] was manipulated to mimic the maternal arterial 
      pH pattern created by ethanol). The experiment was conducted on three consecutive 
      days followed by four days without treatment beginning on gestational day (GD) 
      109, continuing to GD 132. Plasma samples were analyzed for nutrients and 
      metabolites using HPLC and spectrophotometric methods. Maternal plasma 
      concentrations of glutamate increased (58%), whereas glutamine, citrulline, and 
      arginine decreased (between 14 and 53%) in response to an acute challenge after 
      the chronic exposure in ethanol-treated ewes. No differences in these amino acid 
      concentrations were noted between the ethanol and acidemic group subjects. 
      Maternal plasma lactate levels increased by approximately 100% in response to 
      ethanol, whereas glucose and urea levels did not change in any group. We conclude 
      that maternal chronic binge ethanol consumption results in acidosis-mediated 
      reductions in circulating levels of glutamine and related amino acids that could 
      be responsible for neuronal deficits, altered fetal growth, development, and 
      programming. We also speculate that the consequent increase in fetal glutamate 
      during critical periods of brain development may contribute to the pathogenesis 
      of FAS.
FAU - Ramadoss, Jayanth
AU  - Ramadoss J
AD  - Department of Veterinary Physiology and Pharmacology, College of Veterinary 
      Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 
      77843, USA.
FAU - Wu, Guoyao
AU  - Wu G
FAU - Cudd, Timothy A
AU  - Cudd TA
LA  - eng
GR  - R01 AA010940/AA/NIAAA NIH HHS/United States
GR  - R01 AA010940-10/AA/NIAAA NIH HHS/United States
GR  - U01 AA017120/AA/NIAAA NIH HHS/United States
GR  - U01 AA017120-02/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Alcohol
JT  - Alcohol (Fayetteville, N.Y.)
JID - 8502311
RN  - 0 (Amino Acids)
RN  - 0 (Blood Glucose)
RN  - 0RH81L854J (Glutamine)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Acid-Base Equilibrium
MH  - Acidosis/*chemically induced
MH  - Amino Acids/*blood
MH  - Animals
MH  - Blood Glucose/analysis
MH  - Ethanol/*poisoning
MH  - Female
MH  - Glutamine/*blood
MH  - Kidney/physiology
MH  - Muscle, Skeletal/physiology
MH  - Pregnancy
MH  - Pregnancy, Animal/*blood
MH  - Sheep
PMC - PMC2662367
MID - NIHMS83049
EDAT- 2008/11/29 09:00
MHDA- 2009/02/06 09:00
PMCR- 2009/12/01
CRDT- 2008/11/29 09:00
PHST- 2008/03/04 00:00 [received]
PHST- 2008/07/29 00:00 [revised]
PHST- 2008/08/18 00:00 [accepted]
PHST- 2008/11/29 09:00 [pubmed]
PHST- 2009/02/06 09:00 [medline]
PHST- 2008/11/29 09:00 [entrez]
PHST- 2009/12/01 00:00 [pmc-release]
AID - S0741-8329(08)00306-6 [pii]
AID - 10.1016/j.alcohol.2008.08.008 [doi]
PST - ppublish
SO  - Alcohol. 2008 Dec;42(8):657-66. doi: 10.1016/j.alcohol.2008.08.008.