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High-Fat Feeding in Time-Dependent Manner Affects Metabolic Routes Leading to Nervonic Acid Synthesis in NAFLD.

Authors
  • Konstantynowicz-Nowicka, Karolina1
  • Berk, Klaudia2
  • Chabowski, Adrian2
  • Kasacka, Irena3
  • Bielawiec, Patrycja2
  • Łukaszuk, Bartłomiej2
  • Harasim-Symbor, Ewa2
  • 1 Department of Physiology, Medical University of Bialystok, 15-089 Bialystok, Poland. [email protected] , (Poland)
  • 2 Department of Physiology, Medical University of Bialystok, 15-089 Bialystok, Poland. , (Poland)
  • 3 Department of Histology and Cytophysiology, Medical University of Bialystok, 15-089 Bialystok, Poland. , (Poland)
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
Aug 05, 2019
Volume
20
Issue
15
Identifiers
DOI: 10.3390/ijms20153829
PMID: 31387306
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. The disturbances in the fatty acid composition of stored lipids are more important than the lipid species itself, which may influence the overall effect caused by these molecules. Thus, uncovering time-dependent changes in the fatty acid composition of accumulated lipid fractions after a high fat diet seems to be a new marker of NAFLD occurrence. The experiments were conducted on high fat fed Wistar rats. The blood and liver samples were collected at the end of each experimental week and used to assess the content of lipid fractions and their fatty acid composition by gas liquid chromatography. The expression of proteins from lipid metabolism pathways and of fatty acid exporting proteins were detected by Western blotting. In the same high fat feeding period, decreased de novo lipogenesis, increased β-oxidation and lipid efflux were demonstrated. The observed effects may be the first liver protective mechanisms against lipotoxicity. Nevertheless, such effects were still not sufficient to prevent the liver from proinflammatory lipid accumulation. Moreover, the changes in liver metabolic pathways caused the plasma nervonic acid concentration in sphingomyelin to decrease simultaneously with NAFLD development, which may be a steatosis occurrence prognostic marker.

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