Dietary long-chain unsaturated fatty acids acutely and differently reduce the activities of lipogenic enzymes and of citrate carrier in rat liver

J Physiol Biochem. 2016 Sep;72(3):485-94. doi: 10.1007/s13105-016-0495-3. Epub 2016 Jun 16.

Abstract

The activities of lipogenic enzymes appear to fluctuate with changes in the level and type of dietary fats. Polyunsaturated fatty acids (PUFAs) are known to induce on hepatic de novo lipogenesis (DNL) the highest inhibitory effect, which occurs through a long-term adaptation. Data on the acute effects of dietary fatty acids on DNL are lacking. In this study with rats, the acute 1-day effect of high-fat (15 % w/w) diets (HFDs) enriched in saturated fatty acids (SFAs) or unsaturated fatty acids (UFAs), i.e., monounsaturated (MUFA) and PUFA, of the ω-6 and ω-3 series on DNL and plasma lipid level was investigated; a comparison with a longer time feeding (21 days) was routinely carried out. After 1-day HFD administration UFA, when compared to SFA, reduced plasma triacylglycerol (TAG) level and the activities of the lipogenic enzymes acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), a decreased activity of the citrate carrier (CIC), a mitochondrial protein linked to lipogenesis, was also detected. In this respect, ω-3 PUFA was the most effective. On the other hand, PUFA maintained the effects at longer times, and the acute inhibition induced by MUFA feeding on DNL enzyme and CIC activities was almost nullified at 21 days. Mitochondrial fatty acid composition was slightly but significantly changed both at short- and long-term treatment, whereas the early changes in mitochondrial phospholipid composition vanished in long-term experiments. Our results suggest that in the early phase of administration, UFA coordinately reduced both the activities of de novo lipogenic enzymes and of CIC. ω-3 PUFA showed the greatest effect.

Keywords: Citrate carrier; De novo lipogenesis; Dietary fatty acids; High-fat diet; Rat liver.

Publication types

  • Comparative Study

MeSH terms

  • Acetyl-CoA Carboxylase / antagonists & inhibitors
  • Acetyl-CoA Carboxylase / metabolism
  • Animals
  • Carrier Proteins / antagonists & inhibitors*
  • Carrier Proteins / metabolism
  • Diet, High-Fat / adverse effects*
  • Dietary Fats, Unsaturated / adverse effects
  • Dietary Fats, Unsaturated / blood
  • Dietary Fats, Unsaturated / metabolism
  • Dietary Fats, Unsaturated / therapeutic use*
  • Fatty Acid Synthases / antagonists & inhibitors
  • Fatty Acid Synthases / metabolism
  • Fatty Acids, Monounsaturated / adverse effects
  • Fatty Acids, Monounsaturated / blood
  • Fatty Acids, Monounsaturated / metabolism
  • Fatty Acids, Monounsaturated / therapeutic use
  • Fatty Acids, Omega-3 / adverse effects
  • Fatty Acids, Omega-3 / blood
  • Fatty Acids, Omega-3 / metabolism
  • Fatty Acids, Omega-3 / therapeutic use
  • Fatty Acids, Omega-6 / adverse effects
  • Fatty Acids, Omega-6 / blood
  • Fatty Acids, Omega-6 / metabolism
  • Fatty Acids, Omega-6 / therapeutic use
  • Hypertriglyceridemia / blood
  • Hypertriglyceridemia / etiology
  • Hypertriglyceridemia / metabolism
  • Hypertriglyceridemia / prevention & control*
  • Lipids / blood*
  • Lipogenesis*
  • Liver / enzymology
  • Liver / metabolism*
  • Male
  • Mitochondria, Liver / enzymology
  • Mitochondria, Liver / metabolism
  • Phospholipids / metabolism
  • Rats, Wistar
  • Time Factors
  • Triglycerides / antagonists & inhibitors
  • Triglycerides / blood
  • Triglycerides / metabolism

Substances

  • Carrier Proteins
  • Dietary Fats, Unsaturated
  • Fatty Acids, Monounsaturated
  • Fatty Acids, Omega-3
  • Fatty Acids, Omega-6
  • Lipids
  • Phospholipids
  • Triglycerides
  • citrate-binding transport protein
  • Fatty Acid Synthases
  • Acetyl-CoA Carboxylase