Rapid in vivo hydrolysis of fatty acid ethyl esters, toxic nonoxidative ethanol metabolites

Mouris Saghir, Jens Werner, Michael Laposata

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Fatty acid ethyl esters (FAEE), esterification products of fatty acids and ethanol, are in use as fatty acid supplements, but they also have been implicated as toxic mediators of ethanol ingestion. We hypothesized that hydrolysis of orally ingested FAEE occurs in the gastrointestinal (GI) tract and in the blood to explain their apparent lack of toxicity. To study the in vivo inactivation of FAEE by hydrolysis to free fatty acids and ethanol, we assessed the hydrolysis of FAEE administered as an oil directly into the rat stomach and when injected within the core of low-density lipoprotein particles into the circulation of rats. Our studies demonstrate that FAEE are rapidly degraded to free fatty acids and ethanol in the GI tract at the level of the duodenum with limited hydrolysis in the stomach. In addition, FAEE are rapidly degraded in the circulation, with a half-life of only 58 s. Thus the degradation of FAEE in the GI tract and in the blood provides an explanation for the apparent lack of toxicity of orally ingested FAEE.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume273
Issue number1 36-1
StatePublished - Jul 1997
Externally publishedYes

Fingerprint

Poisons
Esters
Hydrolysis
Ethanol
Fatty Acids
Gastrointestinal Tract
Nonesterified Fatty Acids
Stomach
Esterification
LDL Lipoproteins
Duodenum
Half-Life
Oils
Eating

Keywords

  • Alcohol
  • Free fatty acid
  • Omega-3 fatty acids
  • Pancreatitis

ASJC Scopus subject areas

  • Gastroenterology
  • Physiology
  • Physiology (medical)

Cite this

Rapid in vivo hydrolysis of fatty acid ethyl esters, toxic nonoxidative ethanol metabolites. / Saghir, Mouris; Werner, Jens; Laposata, Michael.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 273, No. 1 36-1, 07.1997.

Research output: Contribution to journalArticle

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