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Titolo:
MITOCHONDRION IS THE PRINCIPAL TARGET FOR NUTRITIONAL AND PHARMACOLOGICAL CONTROL OF TRIGLYCERIDE-METABOLISM
Autore:
FROYLAND L; MADSEN L; VAAGENES H; TOTLAND GK; AUWERX J; KRYVI H; STAELS B; BERGE RK;
Indirizzi:
INST NUTR,DIRECTORATE FISHERIES,POB 185 N-5002 BERGEN NORWAY UNIV BERGEN,HAUKELAND HOSP,DEPT BIOL CLIN,DIV BIOCHEM N-5021 BERGEN NORWAY UNIV BERGEN,INST ZOOL N-5007 BERGEN NORWAY INST PASTEUR,DEPT ATHEROSCLEROSE,U325 INSERM F-59019 LILLE FRANCE
Titolo Testata:
Journal of lipid research
fascicolo: 9, volume: 38, anno: 1997,
pagine: 1851 - 1858
SICI:
0022-2275(1997)38:9<1851:MITPTF>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
FATTY-ACID OXIDATION; HEPATIC PEROXISOME PROLIFERATORS; LOW-DENSITY LIPOPROTEIN; APOLIPOPROTEIN C-III; EICOSAPENTAENOIC ACID; DOCOSAHEXAENOIC ACID; FISH-OIL; HYPERLIPIDEMIC PATIENTS; MICRONIZED FENOFIBRATE; HYPOLIPIDEMIC DRUGS;
Keywords:
FISH OIL; FIBRATES; HYPOTRIGLYCERIDEMIC; LIVER; MITOCHONDRIA; MORPHOLOGY; PEROXISOMES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
46
Recensione:
Indirizzi per estratti:
Citazione:
L. Froyland et al., "MITOCHONDRION IS THE PRINCIPAL TARGET FOR NUTRITIONAL AND PHARMACOLOGICAL CONTROL OF TRIGLYCERIDE-METABOLISM", Journal of lipid research, 38(9), 1997, pp. 1851-1858

Abstract

Fish oil polyunsaturated fatty acids and fibrate hypolipidemic drugs are potent hypotriglyceridemic agents that act by increasing fatty acid catabolism and decreasing triglyceride synthesis and secretion by the liver. A major unresolved issue is whether this hypotriglyceridemic effect can occur independent of induction of peroxisomal beta-oxidation, a predisposing factor for hepatocarcinogenesis. The present study was undertaken to determine which component of fish oil, eicosapentaenoic acid (FPA) or docosahexaenoic acid (DHA), is responsible for its triglyceride-lowering effect. We demonstrate that EPA and not DKA is thehypotriglyceridemic component of fish oil and that mitochondria and not peroxisomes are the principal target. Results obtained by fenofibrate feeding support the hypothesis that the mitochondrion is the primary site for the hypotriglyceridemic effect. In contrast to fibrates, EPA did not affect hepatic apolipoprotein C-III gene expression. Therefore, increased mitochondrial beta-oxidation with a concomitant decreasein triglyceride synthesis and secretion seems to be the primary mechanism underlying the hypotriglyceridemic effect of EPA and fibrates in rats, rabbits and possibly also in humans. In addition, these data show that lowering of plasma triglycerides can occur independently of anydeleterious peroxisome proliferation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 08:21:58