A polyphenol extract modifies quantity but not quality of liver fatty acid content in high-fat–high-sucrose diet-fed rats: possible implication of the sirtuin pathway

• Published in: British journal of nutrition Vol. 104; no. 12; pp. 1760 - 1770
• Main Authors: Aoun, Manar, Michel, Francoise, Fouret, Gilles, Casas, Francois, Jullien, Melanie, Wrutniak-Cabello, Chantal, Ramos, Jeanne, Cristol, Jean-Paul, Coudray, Charles, Carbonneau, Marie-Annette, Feillet-Coudray, Christine
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 28.12.2010; Cambridge University Press (CUP)
• Subjects: acetyl-CoA carboxylase; animal models; animal proteins; Animals; biochemical pathways; Biological and medical sciences; Diet; Dietary Fats - administration & dosage; Dietary Fats - adverse effects; Dietary Sucrose - administration & dosage; Dietary Sucrose - adverse effects; enzyme activity; experimental diets; Fatty acids; Fatty Acids - metabolism; fatty liver; Fatty Liver - chemically induced; Feeding. Feeding behavior; Flavonoids - chemistry; Flavonoids - pharmacology; Food and Nutrition; fruit extracts; Fundamental and applied biological sciences. Psychology; gene expression; genes; grapes; high fat diet; High-fat–high-sucrose diet; human diseases; human nutrition; kinases; Life Sciences; Liver; Liver - metabolism; Male; Metabolism and Metabolic Studies; Mitochondria; non-alcoholic fatty liver disease; Nutrition research; Oxidative stress; Phenols - chemistry; Phenols - pharmacology; phospho-acetyl-CoA carboxylase; phosphorylated AMP kinase; phytochemicals; Plant Extracts - chemistry; Plant Extracts - pharmacology; Polyphenols; protein synthesis; Proteins; Random Allocation; Rats; Rats, Wistar; RNA, Messenger - genetics; RNA, Messenger - metabolism; Rodents; Sirtuin 1 - metabolism; Sirtuin-1; sirtuin-1 deacetylase; stearoyl-CoA desaturase; Sucrose; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Sirtuin-1; Polyphenols; Oxidative stress; Mitochondria; Fatty acids; High-fat–high-sucrose diet; Rat; Sucrose; Rodentia; Lipids; Hepatic disease; Quantity; Fat content; Extract; Feeding; Vertebrata; Polyphenol; High-fat-high-sucrose diet; Mammalia; Fatty liver; Diet; Animal; Quality; Fat; Digestive diseases; POLYPHENOLS; OXIDATIVE STRESS; RAT; MITOCHONDRIA; FATTY ACIDS; SIRTUIN-1; HIGH-FAT–HIGH-SUCROSE DIET
• ISSN: 0007-1145; 1475-2662
• DOI: 10.1017/S0007114510002850

High-fat or high-fat–high-sucrose diets are known to induce non-alcoholic fatty liver disease and this is emerging as one of the most common liver diseases worldwide. Some polyphenols have been reported to decrease rat hepatic lipid accumulation, in particular those extracted from red grapes such as resveratrol. The present study was designed to determine whether a polyphenol extract (PPE), from red grapes, modulates liver fatty acid composition and desaturase activity indexes in rats fed a high-fat–high-sucrose (HFHS) diet, and to explore whether sirtuin-1 deacetylase activation was implicated in the effect of the PPE against liver steatosis. The effect of this PPE on mitochondriogenesis and mitochondrial activity was also explored. The PPE decreased liver TAG content in HFHS+PPE diet-fed rats in comparison with HFHS diet-fed rats. The PPE had no effect on liver fatty acid composition, desaturase activity indexes and stearoyl-CoA desaturase 1 (SCD1) gene expression. Sirtuin-1 deacetylase protein expression was significantly increased with the PPE; AMP kinase protein expression was higher with the PPE in comparison with the HFHS rats, but no modification of phosphorylated AMP kinase was observed. Protein expression of phospho-acetyl-CoA carboxylase was decreased in HFHS rats and returned to basal values with the PPE. Finally, the PPE modulated PPARγ coactivator-1α (PGC-1α) but did not modify mitochondriogenesis and mitochondrial activity. In conclusion, the PPE partially prevented the accumulation of TAG in the liver by regulating acetyl-CoA carboxylase phosphorylation, a key enzyme in lipid metabolism, probably via sirtuin-1 deacetylase activation. However, the PPE had no effect on the qualitative composition of liver fatty acids.