Influence of a fat overload on lipogenic regulators in metabolic syndrome patients

Br J Nutr. 2011 Mar;105(6):895-901. doi: 10.1017/S0007114510004514. Epub 2010 Nov 30.

Abstract

Several epidemiological studies have related an increase of lipids in the postprandial state to an individual risk for the development of CVD, possibly due to the increased plasma levels of TAG and fatty acids (FA) through enzymes of FA metabolism. The interaction between nutrition and the human genome determines gene expression and metabolic response. The aim of the present study was to evaluate the influence of a fat overload on the gene mRNA levels of lipogenic regulators in peripheral blood mononuclear cells (PBMC) from patients with the metabolic syndrome. The study included twenty-one patients with criteria for the metabolic syndrome who underwent a fat overload. Measurements were made before and after the fat overload of anthropometric and biochemical variables and also the gene mRNA levels of lipogenic factors. The main results were that the fat overload led to an increased mRNA levels of sterol regulatory element binding protein-1 (SREBP1), retinoid X receptor α (RXRα) and liver X receptor α (LXRα) in PBMC, and this increase was associated with the FA synthase (FASN) mRNA levels. We also found that TAG levels correlated with FASN mRNA levels. In addition, there was a positive correlation of SREBP1 with RXRα and of LXRα with the plasma lipoperoxide concentration. The fat overload led to an increase in regulators of lipogenesis in PBMC from patients with the metabolic syndrome.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Dietary Fats / administration & dosage
  • Dietary Fats / pharmacology*
  • Fatty Acid Synthases / genetics
  • Fatty Acid Synthases / metabolism*
  • Female
  • Humans
  • Leukocytes, Mononuclear / drug effects
  • Lipid Peroxides / blood
  • Lipogenesis / drug effects*
  • Lipogenesis / genetics
  • Lipogenesis / physiology
  • Liver X Receptors
  • Male
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / metabolism*
  • Orphan Nuclear Receptors / biosynthesis*
  • RNA, Messenger / biosynthesis
  • Retinoid X Receptors / biosynthesis*
  • Sterol Regulatory Element Binding Protein 1 / genetics
  • Sterol Regulatory Element Binding Protein 1 / metabolism*
  • Triglycerides / blood

Substances

  • Dietary Fats
  • Lipid Peroxides
  • Liver X Receptors
  • NR1H3 protein, human
  • Orphan Nuclear Receptors
  • RNA, Messenger
  • Retinoid X Receptors
  • Sterol Regulatory Element Binding Protein 1
  • Triglycerides
  • Fatty Acid Synthases