TY - JOUR
T1 - Fatty acid methyl esters are detectable in the plasma and their presence correlates with liver dysfunction
AU - Aleryani, Samir Lutf
AU - Cluette-Brown, Joanne E.
AU - Khan, Zia A.
AU - Hasaba, Hasan
AU - Lopez De Heredia, Luis
AU - Laposata, Michael
N1 - Funding Information:
The authors are grateful to Leonard Tochka and Mara Freimanis in the clinical chemistry laboratory of the MGH for providing the samples. Dr. Aleryani was supported by a Fulbright Association Award (2003–2004) and is a visiting assistant professor, Harvard Medical School. Ms. Katherine Jones reviewed the manuscript for grammar and syntax.
PY - 2005/9
Y1 - 2005/9
N2 - Background: Methanol is a component of certain alcoholic beverages and is also an endogenously formed product. On this basis, we have proposed that methanol may promote synthesis of fatty acid methyl esters (FAMEs) in the same way that ethanol promotes fatty acid ethyl ester (FAEE) synthesis. We tested the hypothesis that FAMEs appear in the blood after ethanol intake. Methods: Patient plasma samples obtained from our laboratory (n = 78) were grouped according to blood ethanol concentrations (intoxicated, blood ethanol > 800 mg/l) and non-intoxicated. These samples were further subdivided into groups based on whether the patient had normal or abnormal liver function tests (abnormal, defined as ≥ 1 abnormality of plasma alanine and aspartate aminotransferase, albumin, total bilirubin, and alkaline phosphatase). A separate set of plasma samples were also divided into normal and abnormal groups based on pancreatic function tests (amylase and lipase). There were no patients with detectable ethanol in this group. Patients with abnormalities in pancreatic function tests were included upon recognition of endogenously produced FAMEs by patients with liver function test abnormalities. FAMEs were extracted from plasma and individual species of FAMEs quantified by gas chromatography-mass spectrometry (GC/MS). Results: Increased concentrations of FAME were found in patient samples with evidence of liver dysfunction, regardless of whether or not they were intoxicated (n = 21, p = 0.01). No significant differences in plasma FAME concentrations were found between patients with normal (n = 15) versus abnormal pancreatic function tests (n = 22, p = 0.72). Conclusions: The presence of FAMEs in human plasma may be related to the existence of liver disease, and not to blood ethanol concentrations or pancreatic dysfunction. The metabolic pathways associated with FAME production in patients with impaired liver function remain to be identified.
AB - Background: Methanol is a component of certain alcoholic beverages and is also an endogenously formed product. On this basis, we have proposed that methanol may promote synthesis of fatty acid methyl esters (FAMEs) in the same way that ethanol promotes fatty acid ethyl ester (FAEE) synthesis. We tested the hypothesis that FAMEs appear in the blood after ethanol intake. Methods: Patient plasma samples obtained from our laboratory (n = 78) were grouped according to blood ethanol concentrations (intoxicated, blood ethanol > 800 mg/l) and non-intoxicated. These samples were further subdivided into groups based on whether the patient had normal or abnormal liver function tests (abnormal, defined as ≥ 1 abnormality of plasma alanine and aspartate aminotransferase, albumin, total bilirubin, and alkaline phosphatase). A separate set of plasma samples were also divided into normal and abnormal groups based on pancreatic function tests (amylase and lipase). There were no patients with detectable ethanol in this group. Patients with abnormalities in pancreatic function tests were included upon recognition of endogenously produced FAMEs by patients with liver function test abnormalities. FAMEs were extracted from plasma and individual species of FAMEs quantified by gas chromatography-mass spectrometry (GC/MS). Results: Increased concentrations of FAME were found in patient samples with evidence of liver dysfunction, regardless of whether or not they were intoxicated (n = 21, p = 0.01). No significant differences in plasma FAME concentrations were found between patients with normal (n = 15) versus abnormal pancreatic function tests (n = 22, p = 0.72). Conclusions: The presence of FAMEs in human plasma may be related to the existence of liver disease, and not to blood ethanol concentrations or pancreatic dysfunction. The metabolic pathways associated with FAME production in patients with impaired liver function remain to be identified.
KW - Alanine aminotransferase
KW - Aspartate aminotransferase
KW - Fatty acid methyl esters
KW - Gas chromatography-mass spectrometry
KW - Liver and pancreatic dysfunction
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U2 - 10.1016/j.cccn.2005.03.038
DO - 10.1016/j.cccn.2005.03.038
M3 - Article
C2 - 15894299
AN - SCOPUS:23644438041
SN - 0009-8981
VL - 359
SP - 141
EP - 149
JO - Clinica Chimica Acta
JF - Clinica Chimica Acta
IS - 1-2
ER -