Premium
Sex‐ and Drinking History Dysregulate ω‐3 and ω‐6 Pathways during the Onset of Liver injury in Very Heavy Drinking Alcohol Dependents
Author(s) -
Song Ming,
Vatsalya Vatsalya,
Schwandt Melanie,
Barve Shirish,
Cave Matthew,
George David,
McClain Craig
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1020.7
Subject(s) - liver injury , medicine , fatty liver , alcohol , physiology , heavy drinking , gastroenterology , endocrinology , poison control , injury prevention , chemistry , biochemistry , environmental health , disease
Background/Aims Heavy alcohol drinking causes liver injury. In this study we aim to study the relation between gender, drinking history and fatty acids and the severity of liver injury. Methods 114 heavy drinking alcohol dependent (AD) patients in the 21–65 years old were recruited, including 74 males and 40 females. Patients were divided into two groups: non‐elevated liver‐injury (NELI) group with ALT蠄 40IU/L, and elevated liver‐injury (ELI) group with ALT >40IU/L. Chem20, ω‐3 and ω‐6 fatty acids were evaluated. Results In ELI group, 40 are males, 16 are females. Females showed more severe liver injury than males, as demonstrated by markedly higher serum AST and LDH. Drinking history measurement showed significant predictability for the fatty acids involved in the pro‐inflammatory and protective pathways. Most of the fatty acids in ω‐3 pathway were increased in males, but not in females in ELI group compared to those in NELI group. ω‐3 and ω‐6 pathway regulation showed differences in response with drinking history that was closely associated with its unique markers. Conclusions Variability in response to pro‐inflammatory and protective mechanism of fatty acid pathways represent susceptibility in the immune response and liver injury in patients with heavy alcohol drinking that may require specific medical management.