Platelet-activating factor modulates fat storage in the liver induced by a high-refined carbohydrate-containing diet

J Nutr Biochem. 2015 Sep;26(9):978-85. doi: 10.1016/j.jnutbio.2015.04.004. Epub 2015 May 10.

Abstract

Hepatic diseases are comorbidities caused by obesity and are influenced by diet composition. The aim of this study was to evaluate the kinetics of metabolic and inflammatory liver dysfunction induced by a high-refined carbohydrate-containing (HC) diet and to determine how platelet-activating factor (PAF) modulates the liver lipid content of mice. BALB/c mice were fed a chow or HC diet for the following experimental periods: 1 and 3 days, 1, 2, 4, 6, 8, 10 and 12 weeks. Wild-type (WT) and PAF receptor-deficient (PAFR(-/-)) mice were fed the same diets for 8 weeks. Mice fed with HC diet showed higher triglycerides and cholesterol levels, fibrosis and inflammation in the liver. The number of neutrophils migrating into the liver was also increased in mice fed with HC diet. However, transaminase levels did not change. PAFR(-/-) mice fed with HC diet showed more steatosis, oxidative stress and higher transaminases levels associated with lower inflammation than WT mice. The consumption of HC diet altered the metabolic and inflammatory response in the liver and was worse in PAFR(-/-) mice. We suggest that PAF regulates liver lipid content and dyslipidemia, protecting the mice from lipotoxicity and liver damage.

Keywords: Collagen deposition; Dyslipidemia; Inflammation; Liver; Steatosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cholesterol / blood
  • Cholesterol / metabolism
  • Dietary Carbohydrates / adverse effects*
  • Dyslipidemias / etiology
  • Dyslipidemias / immunology
  • Dyslipidemias / metabolism
  • Dyslipidemias / pathology
  • Food Handling
  • Lipid Metabolism*
  • Lipid Peroxidation
  • Liver / immunology
  • Liver / metabolism*
  • Liver / pathology
  • Liver Cirrhosis / etiology
  • Male
  • Mice, Inbred BALB C
  • Mice, Knockout
  • Neutrophil Infiltration
  • Non-alcoholic Fatty Liver Disease / etiology
  • Non-alcoholic Fatty Liver Disease / immunology
  • Non-alcoholic Fatty Liver Disease / metabolism*
  • Non-alcoholic Fatty Liver Disease / pathology
  • Oxidative Stress
  • Platelet Activating Factor / metabolism*
  • Platelet Membrane Glycoproteins / agonists*
  • Platelet Membrane Glycoproteins / genetics
  • Platelet Membrane Glycoproteins / metabolism
  • Receptors, G-Protein-Coupled / agonists*
  • Receptors, G-Protein-Coupled / blood
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / metabolism
  • Signal Transduction*
  • Time Factors
  • Triglycerides / blood
  • Triglycerides / metabolism

Substances

  • Dietary Carbohydrates
  • Platelet Activating Factor
  • Platelet Membrane Glycoproteins
  • Receptors, G-Protein-Coupled
  • Triglycerides
  • platelet activating factor receptor
  • Cholesterol