title: Dietary saturated fatty acids reduce hepatic lipid accumulation but induce fibrotic change in alcohol-fed rats.
abstract: BACKGROUND
  In this study, we evaluated the influence of an ethanol-containing diet with high saturated fatty acids (SFAs) on alcoholic liver disease (ALD) in rats.
  
  
  METHODS
  Male Wistar rats weighing about 160 g were divided into four groups: an ethanol (E) group fed an ethanol-containing liquid diet with 36% total calories as fat (corn oil, olive oil and safflower oil); a control (C) group pair-fed an isoenergetic diet without ethanol; an ethanol with saturated fat (EHS) group fed an ethanol-containing diet which contained 40% total calories as fat (90% lard); and a control with saturated fat (CHS) group fed an isoenergetic diet without ethanol, which contained 40% total calories as fat.
  
  
  RESULTS
  After 8 weeks of treatment, the liver weight and plasma aspartate aminotransferase (AST) activities in E and EHS groups were significantly higher than those of C group. Significantly higher scores of inflammation, necrosis, and fatty changes were found in E group, whereas significantly higher scores of necrosis, bile duct hyperplasia, and fibrosis were found in EHS group. Although significantly lower plasma adiponectin concentrations were observed in both E and EHS groups, compared to C group, plasma adiponectin in EHS group was significantly higher than that in E group. There was no change in hepatic peroxisome proliferator activated receptor (PPAR)-α expression between E and C groups, and rats in EHS group showed a significantly elevated level compared to the other groups. A lower hepatic sirtuins (SIRT)-1 level was found in E group, but it did not reach statistical significance. Moreover, the highest plasma TGF-β1 level was found in EHS group. Compared to C group, the hepatic reduced glutathione/oxidized glutathione ratio and thiobarbituric acid (TBA)-reactive substance level were significantly increased in E and EHS groups; however, there was no significant difference between E and EHS groups. Significantly increased hepatic CYP2E1 expression was observed in both E and EHS groups, while at the same time, hepatic CYP2E1 in EHS group was the highest among all groups. The hepatic tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 concentrations in the E group were significantly higher than those in C group, whereas the hepatic IL-6 and IL-10 concentrations in ES group were significantly lower than those of E group.
  
  
  CONCLUSIONS
  These results suggested that dietary saturated fats may inhibit hepatic fat accumulation and induce hepatic fibrosis in rats under chronic alcohol intake.
authors.affiliation: 1 School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan ; 2 Nutrition and Cancer Biology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111-1524, USA.
authors.forename: Ya-Ling
authors.initials: YL
authors.lastname: Chen
authors.affiliation: 1 School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan ; 2 Nutrition and Cancer Biology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111-1524, USA.
authors.forename: Hsiang-Chi
authors.initials: HC
authors.lastname: Peng
authors.affiliation: 1 School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan ; 2 Nutrition and Cancer Biology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111-1524, USA.
authors.forename: Xiang-Dong
authors.initials: XD
authors.lastname: Wang
authors.affiliation: 1 School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan ; 2 Nutrition and Cancer Biology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111-1524, USA.
authors.forename: Suh-Ching
authors.initials: SC
authors.lastname: Yang
keywords: Alcoholic liver disease (ALD); lard; rats; saturated fatty acid (SFA)