Lipids

, Volume 47, Issue 10, pp 941–950

Dietary trans-Fatty Acid Induced NASH is Normalized Following Loss of trans-Fatty Acids from Hepatic Lipid Pools

  • Brent A. Neuschwander-Tetri
  • David A. Ford
  • Sahaja Acharya
  • George Gilkey
  • Metin Basaranoglu
  • Laura H. Tetri
  • Elizabeth M. Brunt
Original Article

DOI: 10.1007/s11745-012-3709-7

Cite this article as:
Neuschwander-Tetri, B.A., Ford, D.A., Acharya, S. et al. Lipids (2012) 47: 941. doi:10.1007/s11745-012-3709-7

Abstract

Previous experiments in mice showed that dietary trans-fats could play a role in non-alcoholic steatohepatitis (NASH) yet little is known about the accumulation trans-fats in hepatic lipid pools in relationship to liver injury. NASH is also associated with obesity yet improves with only modest weight loss. To distinguish the role of obesity versus sustained consumption of a trans-fat containing diet in causing NASH, mice with obesity and NASH induced by consuming a high trans-fat diet for 16 weeks were subsequently fed standard chow or maintained on trans-fat chow for another 8 weeks. The accumulation, partitioning and loss of trans-fats in the major hepatic lipid pools during and after trans-fat consumption were determined. Obese mice switched to standard chow remained obese but steatohepatitis improved. trans-fats were differentially incorporated into the major hepatic lipid pools and the loss of trans-fats after crossover to control chow was greatest in the cholesteryl ester pool. In summary, dietary changes can improve the biochemical and histopathological changes of NASH despite persistent obesity in mice. Analysis of hepatic lipids confirmed that dietary trans-fats accumulate in the major lipid pools and are released differentially with diet normalization. The substantial loss of trans-fats from the cholesteryl ester pool in parallel with improvement in NASH suggests that this pool of trans-fats could play a role in the pathogenesis of NASH.

Keywords

High fructose corn syrup Fatty liver Obesity Leptin Resistin 

Abbreviations

NASH

Nonalcoholic steatohepatitis

ALIOS

American lifestyle induced obesity syndrome

ALT

Alanine aminotransferase

MUFA

Monounsaturated fatty acid(s)

PUFA

Polyunsaturated fatty acid(s)

HFCS

High fructose corn syrup

EDTA

Ethylenediaminetetraacetic acid

FAME

Fatty acid methyl ester(s)

VLDL

Very low density lipoprotein

SCD

Stearoyl-CoA desaturase

XO

Crossover

Copyright information

© AOCS 2012

Authors and Affiliations

  • Brent A. Neuschwander-Tetri
    • 1
    • 2
    • 7
  • David A. Ford
    • 3
    • 4
  • Sahaja Acharya
    • 5
  • George Gilkey
    • 5
  • Metin Basaranoglu
    • 1
  • Laura H. Tetri
    • 1
  • Elizabeth M. Brunt
    • 6
  1. 1.Division of Gastroenterology and Hepatology, Department of Internal MedicineSaint Louis UniversitySaint LouisUSA
  2. 2.Liver CenterSaint Louis UniversitySaint LouisUSA
  3. 3.Department of Biochemistry and Molecular BiologySaint Louis UniversitySaint LouisUSA
  4. 4.Center for Cardiovascular ResearchSaint Louis UniversitySaint LouisUSA
  5. 5.School of MedicineSaint Louis UniversitySaint LouisUSA
  6. 6.Department of Pathology and ImmunologyWashington UniversitySaint LouisUSA
  7. 7.Saint LouisUSA 

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