scholarly journals Fatty acid ethyl ester synthase, an enzyme for nonoxidative ethanol metabolism, is present in serum after liver and pancreatic injury

1996 ◽  
Vol 42 (1) ◽  
pp. 24-27 ◽  
Author(s):  
S Aleryani ◽  
A Kabakibi ◽  
J Cluette-Brown ◽  
M Laposata

Abstract Fatty acid ethyl esters (FAEE), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol-induced organ damage. Because cytosolic enzymes such as aspartate aminotransferase, lipase, and amylase appear in the blood after liver or pancreatic damage, we hypothesized that FAEE synthase, which is both cytosolic and membrane bound, is also released into the blood of patients with liver or pancreatic disease. We used a method involving thin-layer chromatography coupled with gas chromatography-mass spectrometry to reliably identify and quantify FAEE. In this study, we demonstrated that patients with liver or pancreatic disease release FAEE synthase into their plasma in amounts proportional to the amount of aspartate aminotransferase (r = 0.78), amylase (r = 0.65), and lipase (r = 0.63). These data indicate that liver and pancreatic damage results in release of FAEE synthase into the blood. The presence of FAEE synthase in plasma permits nonoxidative ethanol metabolism in the plasma.

Jurnal Kimia ◽  
2020 ◽  
pp. 175
Author(s):  
N. M. Suaniti ◽  
I W. Wiratama ◽  
I. E. Suprihatin

Fatty acid ethyl ester (FAEE) merupakan salah satu biomarker konsumsi etanol. Penelitian ini bertujuan untuk menganalisis senyawa FAEE dalam sampel rambut secara kualitatif dengan GC-MS. Pada penelitian ini dibuat campuran standar FAEE (Etil Pamlitat dan Etil Oleat) 100 ppm dengan perbandingan 1:1 kemudian dibuat variasi konsentrasi. Metode validasi standar FAEE diukur menggunakan GC-MS. Sampel rambut dipreparasi dengan cara didekontaminasi kemudian diekstraksi dan diinjeksikan ke sistem GC-MS. Hasil validasi diperoleh persamaan regresi linier yaitu, y = 240713,507x-147471,2353 untuk etil palmitat dan y = 58361,45x+242,5 untuk etil oleat dengan nilai koefisien korelasi (r2) berturut-turut sebesar 0,9996 dan 0,9999. Batas deteksi diperoleh sebesar 2,5522 ppm dan 0,0189 ppm, dengan batas kuantitasi sebesar 8,5073 ppm dan 0,0630 ppm. Nilai koefisien variansi diperoleh sebesar 3,59% dan 8,65 x 10-4%, dengan persen perolehan kembali sebesar 100,05% dan 100,08%. Hasil analisis menunjukkan, sampel rambut semua sukarelawan mengandung etil palmitat dan etil oleat pada waktu retensi 22,03 menit dan 23,83 menit. Kata kunci: Fatty acid ethyl esters, Etil Palmitat, Etil Oleat, Alkohol, Etanol, Biomarker, GC-MS


1997 ◽  
Vol 43 (8) ◽  
pp. 1527-1534 ◽  
Author(s):  
Michael Laposata

Abstract This review includes a description of short-term and long-term markers of ethanol intake and their clinical utility. The major portion of this report is a summary of studies on fatty acid ethyl ester, a new marker for monitoring both acute and chronic ethanol intake. With the markers described in the review, algorithms to assess recent ethanol intake, chronic ethanol intake, and end organ damage are included to provide a practical approach to the evaluation of the patient.


1992 ◽  
Vol 185 (3) ◽  
pp. 938-943 ◽  
Author(s):  
Keith E. Isenberg ◽  
Puran S. Bora ◽  
Xia Zhou ◽  
Xiaolin Wu ◽  
Blake W. Moore ◽  
...  

1997 ◽  
Vol 113 (1) ◽  
pp. 286-294 ◽  
Author(s):  
J Werner ◽  
M Laposata ◽  
C Fernandez-del Castillo ◽  
M Saghir ◽  
RV Iozzo ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. G65-G73 ◽  
Author(s):  
Jens Werner ◽  
Mouris Saghir ◽  
Andrew L. Warshaw ◽  
Kent B. Lewandrowski ◽  
Michael Laposata ◽  
...  

The mechanism by which alcohol injures the pancreas remains unknown. Recent investigations suggest a role for fatty acid ethyl ester (FAEE), a nonoxidative metabolite of ethanol, in the pathogenesis of alcohol pancreatitis. In this study, we characterized ethanol-induced injury in rats and evaluated the contribution of oxidative and nonoxidative ethanol metabolites in this form of acute pancreatitis. Pancreatic injury in rats was assessed by edema, intrapancreatic trypsinogen activation, and microscopy after infusing ethanol with or without inhibitors of oxidative ethanol metabolism. Plasma and tissue levels of FAEE and ethanol were measured and correlated with pancreatic injury. Ethanol infusion generated plasma and tissue FAEE and, in a dose-dependent fashion, induced a pancreas-specific injury consisting of edema, trypsinogen activation, and formation of vacuoles in the pancreatic acini. Inhibition of the oxidation of ethanol significantly increased both FAEE concentration in plasma and pancreas and worsened the pancreatitis-like injury. This study provides direct evidence that ethanol, through its nonoxidative metabolic pathway, can produce pancreas-specific toxicity in vivo and suggests that FAEE are responsible for the development of early pancreatic cell damage in acute alcohol-induced pancreatitis.


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