出版社：American Society for Biochemistry and Molecular Biology
摘要：Fifteen weeks of dietary n-3 PUFA deprivation increases coefficientsof conversion of circulating -linolenic acid (-LNA; 18:3n-3)to docosahexaenoic acid (DHA; 22:6n-3) in rat liver but notbrain. To determine whether these increases reflect organ differencesin enzymatic activities, we examined brain and liver expressionof converting enzymes and of two of their transcription factors,peroxisome proliferator-activated receptor (PPAR) and sterol-regulatoryelement binding protein-1 (SREBP-1), in rats fed an n-3 PUFA"adequate" (4.6% -LNA of total fatty acid, no DHA) or "deficient"(0.2% -LNA, no DHA) diet for 15 weeks after weaning. In ratsfed the deficient compared with the adequate diet, mRNA andactivity levels of 5 and 6 desaturases and elongases 2 and 5were upregulated in liver but not brain, but liver PPAR andSREBP-1 mRNA levels were unchanged. In rats fed the adequatediet, enzyme activities generally were higher in liver thanbrain. Thus, differences in conversion enzyme expression explainwhy the liver has a greater capacity to synthesize DHA fromcirculating -LNA than does the brain in animals on an adequaten-3 PUFA diet and why liver synthesis capacity is increasedby dietary deprivation. These data suggest that liver n-3 PUFAmetabolism determines DHA availability to the brain when DHAis absent from the diet.Supplementary key words ß-oxidation • diet • docosahexaenoic acid • -linolenic acid • polyunsaturated fatty acid
Abbreviations: AA, arachidonic acid (20:4n-6); CPT-1, carnitine palmitoyltransferase-1; DHA, docosahexaenoic acid (22:6n-3); DPA, docosapentaenoic acid (22:5n-6); DTA, docosatetraenoic acid (22:4n-6); EPA, eicosapentaenoic acid (20:5n-3); FAME, fatty acid methyl ester; KPB, potassium phosphate buffer; LA, linoleic acid (18:2n-6); -LNA, -linolenic acid (18:3n-3); PPAR, peroxisome proliferator-activated receptor; PUFA, polyunsaturated fatty acid; SREBP, sterol-regulatory element binding protein
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