Prostaglandins, Leukotrienes and Essential Fatty Acids
Dietary alpha-linolenic acid enhances omega-3 long chain polyunsaturated fatty acid levels in chicken tissues☆
Introduction
The beneficial health effects of dietary omega-3 (n−3) long chain polyunsaturated fatty acids (LCPUFA), especially eicosapentaenoic acid (EPA, 20:5n−3), docosapentaenoic acid (DPA, 22:5n−3) and docosahexaenoic acid (DHA, 22:6n−3) have been well documented [1], [2], [3], [4], [5], [6]. One approach to increase the dietary n−3 LCPUFA intake of humans is to increase the intake of fish which is known as the main dietary source of n−3 LCPUFA. However, as many people in Western societies consume very little fish, increasing the levels of n−3 LCPUFA in foods eaten in large amounts including chicken meat may be an alternative strategy to increase n−3 LCPUFA consumption without changing existing dietary habits. The success of this strategy would depend on developing ways to increase the n−3 LCPUFA content of chicken meat above current levels.
Several studies have demonstrated that it is possible to increase the level of n−3 LCPUFA in chicken meat through supplementation of the diet with fish oil [7], [8], [9], [10]. However, the use of fish oil in the manipulation of chicken meat fatty acid composition may result in negative effects on the sensory properties of meat [7], [11], [12]. An alternative is to enhance the natural production of n−3 LCPUFA in chickens by incorporating vegetable oils rich in the n−3 precursor, alpha-linolenic acid (ALA, 18:3n−3), in their diets. Vegetable oils such as flaxseed and canola are rich sources of ALA. While some authors [13], [14], [15] have reported an increase in chicken meat EPA, DPA and DHA following the consumption of diets rich in ALA, others have failed to demonstrate an increase in n−3 LCPUFAs in tissues [16], [17]. The reasons for these variable responses remain unclear.
The conversion of ALA into n−3 LCPUFA is influenced by the availability of substrate and levels of desaturation and elongation enzymes located in liver. However, because these same enzymes are also involved in the conversion of the n−6 PUFA, linoleic acid (LA, 18:2n−6), to arachidonic acid (AA, 20:4n−6), there is potential for competitive inhibition between n−6 and n−3 PUFA in the diet [18], [19]. Hence, high dietary consumption of LA has the potential to reduce the production of EPA and DHA and favour a high conversion to AA simply by competitively inhibiting ALA access to key enzymes such as delta 6 desaturase [20]. Thus, a major determinant for the optimal conversion of ALA is the ratio of LA to ALA in the diet.
The objective of this study was to examine the effect of increasing dietary ALA content on the conversion of ALA into EPA, DPA and DHA by measuring their accumulation in chicken meat (breast and thigh) when the level of competing substrate, LA, was kept relatively constant.
Section snippets
Birds and diets
This study was approved by the Animal Ethics Committees of the Department of Primary Industries and Resources South Australia and the University of Adelaide. Sixty unsexed one-day-old broiler chickens (Cobb 500) obtained from the Baiada hatchery (Willaston, South Australia, Australia) were randomly allocated to one of six diets (n=10 birds/diet). The birds were reared at the Pig and Poultry Production Institute (PPPI), South Australian Research and Development Institute (SARDI), Roseworthy
Growth parameters
There was no statistical difference in the weights of the birds in any of the dietary treatments at 28 day of age. The average weight of the chickens (n=6) in each group fed with control diet, and diets 1–5 was 1393, 1504, 1482, 1434, 1470 and 1361g, respectively (SEM=50.5).
Liver phospholipid fatty acids
The fatty acid composition of PL in liver samples is shown in Table 3. Increasing levels of dietary ALA from 0.3 to 8%en did not affect the total fat content of liver tissues but elevated the ALA content from 0.2% in control
Discussion and conclusion
The results of this study showed that increasing the levels of dietary ALA from approximately 0.3 to 8%en produced an increase in the accumulation of EPA, DPA and DHA n−3 LCPUFAs in chicken meat of between 4- and 9-fold compared to the ‘control’ birds. It is important to note that the fatty acid composition of the control diet was close to a typical commercial feed and therefore these birds produced near industry standard meat as regards n−3 LCPUFA content. The n−3 LCPUFA accumulation in meat
Acknowledgements
The authors would like to thank Dr. John Carragher for the constructive comments, Prof. Martine Boulianne (SARDI Visiting Scientist from the University of Montreal, Canada), Mr Greg Connors and Ridley Agriproduct Pty Ltd, Murray Bridge, Australia, Mr David Apps, Mr Derek Schultz, Ms Evelyn Daniels, Ms Kylee Swanson, Ms Natasha Edwards, Ms Wei-Chun Tu and Ms Ella Zielinski for technical support, and the SARDI Pig and Poultry Production Institute, Roseworthy Campus for help in conducting the
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Supported by the Australian Agency for International Development (AusAID) and intramural funds from the University of Adelaide. R.A. Gibson and M. Makrides were supported in part by the National Health and Medical Research Council of Australia.