N-6 and N-3 PUFA in liver lipids, thromboxane formation and blood pressure from SHR during diets supplemented with evening primrose, sunflowerseed or fish oil

Abstract

Spontaneously hypertensive rats (SHR) after weaning (at 4 weeks of age) were fed diets supplemented with either sunflowerseed oil (SO), evening primrose oil (EPO), fish oil (FO) or EPO + FO (50%:50 %, v v ) for 22 weeks. A diet with commercially available pellets served as control. Systolic blood pressure was significantly lower in the dietary groups receiving FO, EPO and FO + EPO, the former being most effective. In liver triglycerides (TG) EPO resulted in a markedly increased percentage of linoleic acid (LA; C 18:2, n-6), α-linolenic acid (α-LNA; C 18:3, n-6) and especially of arachidonic acid (AA; C 20:4, n-6), whereas the long-chain n-3 polyunsaturated fatty acids (PUFA), eicosapentaenoic acid (EPA; C 20:5, n-3) and docosahexaenoic acid (DHA; C 22:6 n-3), were depressed to undetectable and significantly lower levels, respectively. In liver phosphatidylcholine (PC) and phosphatidylethanolamine (PE) only slight changes of LA and AA were observed. Feeding of FO led to a significant rise of EPA and DHA in liver TG, PC and PE at the expense of n-6 PUFA (except LA in PC and PE). With a combination of both EPO and FO a significant increase of EPA and DHA, but on lower levels as compared to FO alone, was associated with a significant rise of LA, but with a slight decline of AA as compared to the control animals. Nevertheless, the levels of AA in the group fed EPO + FO were still higher than in the FO-group. In the SO-group the increase of LA was even higher when compared with the EPO-group. The concomitant rise of AA in liver was, however, minor and of similar magnitude in liver PC and PE in comparison to the EPO-group. The thromboxane B 2-formation in serum from SHR appeared markedly depressed during FO feeding, but was augmented during EPO- and SO-rich diet. Although the diets were not adjusted to equimolar amounts of n-6 and n-3 PUFA, the data indicate that the highest supply of the prostaglandin precursors AA and EPA can be obtained when the long-chain n-6 and n-3 PUFA, being able to by-pass the delta-6-desaturase level, are provided. There is increasing evidence that not the C 18-PUFA, but their C 20-homologues are the biologically most effective dietary PUFA, from which those of the n-3 family are abundant and easily available in natural sources, such as food of marine origin. The simultaneous dietary intake of n-6 and n-3 PUFA can overbalance the probably detrimental depression of n-6 PUFA, when n-3 PUFA are fed alone. To find the best dietary n-3 n-6 ratio is one of the urgent demands of recommendations for preventive and/or therapeutic strategies to reduce the cardiovascular risk.