학술논문

Plasma Oxylipin Profile Discriminates Ethnicities in Subjects with Non-Alcoholic Steatohepatitis: An Exploratory Analysis
Document Type
article
Source
Metabolites. 12(2)
Subject
Medical Biochemistry and Metabolomics
Biomedical and Clinical Sciences
Chronic Liver Disease and Cirrhosis
Hepatitis
Cannabinoid Research
Endocannabinoid System Research
Digestive Diseases
Liver Disease
2.1 Biological and endogenous factors
Obesity
Nutrition
Metabolic and endocrine
Oral and gastrointestinal
arachidonic acid
Caucasian
cyclooxygenases
endocannabinoids
ethnicity
Hispanic
lipoxygenases
non-alcoholic steatohepatitis
oxylipins
polyunsaturated fatty acids
soluble epoxide hydrolases
Analytical Chemistry
Biochemistry and Cell Biology
Clinical Sciences
Biochemistry and cell biology
Medical biochemistry and metabolomics
Analytical chemistry
Language
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a common liver pathology that includes steatosis, or non-alcoholic fatty liver (NAFL), and non-alcoholic steatohepatitis (NASH). Without a clear pathophysiological mechanism, it affects Hispanics disproportionately compared to other ethnicities. Polyunsaturated fatty acids (PUFAs) and inflammatory lipid mediators including oxylipin (OXL) and endocannabinoid (eCB) are altered in NAFLD and thought to contribute to its pathogenesis. However, the existence of ethnicity-related differences is not clear. We employed targeted lipidomic profiling for plasma PUFAs, non-esterified OXLs and eCBs in White Hispanics (HIS, n = 10) and Caucasians (CAU, n = 8) with biopsy-confirmed NAFL, compared with healthy control subjects (HC; n = 14 HIS; n = 8 CAU). NAFLD was associated with diminished long chain PUFA in HIS, independent of histological severity. Differences in plasma OXLs and eCBs characterized ethnicities in NASH, with lower arachidonic acid derived OXLs observed in HIS. The secondary analysis comparing ethnicities within NASH (n = 12 HIS; n = 17 CAU), confirms these ethnicity-related differences and suggests lower lipoxygenase(s) and higher soluble epoxide hydrolase(s) activities in HIS compared to CAU. While causes are not clear, these lipidomic differences might be with implications for NAFLD severity and are worth further investigation. We provide preliminary data indicating ethnicity-specific lipidomic signature characterizes NASH which requires further validation.