Omega-3 fatty acids in broiler breeder diets – fad or future?

In recent years, there has been interest in increasing the levels of the n-3 (omega-3) series of long-chain polyunsaturated fatty acids (PUFA) in animal diets by adding fish oil, flax seed and other sources of n-3 fatty acids (Givens et al., 2006; Wiseman, 1997).

This interest was stimulated by studies that showed that inclusion of n-3 fatty acids in human diets has a positive effect on health, such as reducing plasma triglyceride levels and the risk of cardiovascular and other diseases (Ignarro et al., 2007; Mazza et al., 2007). The interest is also based on earlier studies that showed the addition of n-3 fatty acids to benefit animal health (Wang et al., 2000; Wang et al., 2004).

Polyunsaturated fatty acids of the n-3 and n-6 series are the major constituents of embryonic tissues (Speake et al., 1998) and have a number of important roles, many related to the structure and function of cell membranes and the production of eicosanoids, a family of hormone-like compounds derived from arachidonic acid (C20:4(n-6)); two important types of eicosanoids are prostaglandins and leukotrienes (Manev and Uz, 2003).

In addition, an adequate supply of the essential fatty acids, linoleic (C18:2(n-6)) and α-linolenic acid (C18:3(n-3)), is especially important during development, since high content of docosahexaenoic fatty acid (C22:6(n-3), DHA) is required in the phospholipids of the neuronal membranes (Speake et al., 1998). Because polyunsaturated fatty acids are susceptible to oxidation, this increases the requirement for antioxidants in diets (Henning et al., 2001; Surai, 2005).

Linoleic acid is the main fatty acid component in standard cereal-based poultry diets, thus commercial poultry diets are characterized by a high concentration of n-6 fatty acids. However, studies using both wild and captive birds have shown that feral species, which are free to select their diets from the environment, lay eggs that have a high concentration of n-3 fatty acids (Decrock et al., 2001; Speake et al., 1999; Speake and Wood, 2005). It is not clear what the optimal concentrations of n-3 and n-6 fatty acids are in the chicken egg.


PUFA and progeny

Apart from gas exchange, the bird’s egg is a closed system. Thus, all of the nutrients required by the growing embryo and deposited in the egg originate in the maternal diet, which is why broiler breeder nutrition has an important effect on chicks.

In recent years, maternal nutrition and its impact on progeny nutritional status, health and performance have received considerable attention. For example, chicks hatched from breeders fed diets with a low ratio of linoleic:α-linolenic acid were found to have a higher concentration of circulating immunoglobulin G compared with chicks hatched from hens fed diets with a high ratio of linoleic:α-linolenic acid (Wang et al., 2004).

Thus, the addition of the n-3 and n-6 series of PUFA to the maternal diet can affect the passive immunity of the progeny (Wang et al., 2004). Hall et al. (2007) reported that progeny originating from breeders fed fish oil, rich in n-3 fatty acids, and fed a diet devoid of eicosopentaenoic acid (C20:5(n-3), EPA) and DHA, produced a different type of leukotriene than chicks fed the same diet devoid of EPA and DHA but originating from breeders fed sunflower oil, which is rich in n-6 fatty acids. Thus, the PUFA composition of the maternal diet can alter the type of leukotriene produced in chick tissues and could lead to lower incidence of inflammatory disorders in broiler birds.


PUFA and antioxidants in breeder diets

Birds have evolved an antioxidant defence system that can preserve the integrity of PUFA. Tocopherol (vitamin E) and selenium (Se) are key components of that system, reducing lipid peroxidation (Surai et al., 1999a; Surai, 2001; Surai, 2002). Thus, antioxidants can provide better conditions during embryogenesis and hatching by protecting tissues from oxidation and maintaining the level of PUFA, such as DHA, in tissues.

Surai (1999) reported that the concentration of tocopherol in the liver increases during the last weeks of incubation probably to protect the PUFA that have accumulated in embryonic tissues. In contrast, the concentration of vitamin E declines abruptly during the first two weeks post-hatch. It seems that the reserves accumulated in the liver during embryonic development are used by chickens during this period (Cherian and Sim, 2003; Surai et al., 1999b).

Cherian and Sim (2003) fed breeders diets containing 3.5% menhaden oil (MO), linseed oil (LO), or sunflower oil (SO) and 400 μg/g tocopherol. They found that, at hatch, chicks from the MO-fed hens had the lowest liver and plasma tocopherol concentrations. Probably tocopherol was used to protect the high amounts of n-3 PUFA found in tissues of chicks originating from hens fed MO.

The same authors concluded that PUFA in the maternal diet could alter the tocopherol status of chicks in early life.

Inclusion of PUFA and selenium in the maternal diet can have an effect on embryo viability, hatchability and growth of the progeny (Pappas et al., 2005; Pappas et al., 2006a; b). In detail, prepeak (23 wk) and peak (27 wk) production breeders were fed one of four diets: a wheat-based commercial breeder diet with 55 g/kg of either soybean oil (SO) or fish oil (FO), but no added selenium (only that originating from feed ingredients), and each diet with added selenium as Sel-Plex® (Alltech Inc.; SO + Se, FO + Se).

The diets were designed to contain <0.1 mg/kg Se and about 0.5 mg/kg Se for the non-supplemented (no added Se) and the supplemented diets, respectively. The high level of fish oil included in the breeder diet increased embryonic mortality in week 3 of incubation and reduced hatchability and day-old chick weight in hens of both ages.

However, the addition of selenium to the FO diets ameliorated some of these effects, because chicks hatched from eggs laid by 23-week-old breeders on the FO + Se treatment were heavier than those originating from breeders fed the FO treatment.

The effects of maternal nutrition on the concentration of DHA of the progeny persisted for 14 days post–hatch; during that period, chicks from hens fed diets high in PUFA had higher concentrations of DHA in the brain and liver compared with chicks hatched from hens fed diets low in PUFA. The DHA content of the tissues of chicks from breeders fed diets supplemented with selenium was higher than that of chicks from breeders fed unsupplemented diets, indicating that supplementation of the maternal diet with selenium appears to enhance the DHA concentration of the chick brain, which may improve brain function.

It seems likely that a combination of antioxidants such as organic selenium and high levels of vitamin E in breeder diets might further protect PUFA in embryonic tissues compared with that of selenium or tocopherol supplementation alone. Surai (2000) showed that a combination of Sel-Plex® organic selenium supplementation with high levels of vitamin E further increased glutathione (an antioxidant enzyme) concentration in the liver of chickens compared with that of selenium supplementation alone.

As previously mentioned, feral species lay eggs that have a high concentration in n-3 fatty acids. It is possible that these birds may also consume high levels of antioxidants to protect the n-3 fatty acid content of the eggs. Indeed, when recently we measured the yolk selenium concentrations in eggs of 14 avian species collected in the wild, we found that the concentration of selenium in egg yolks varied from 394 to 2238 ng/g.

Selenium concentration in egg yolk of the domestic chicken is only about 100 ng/g yolk when birds are fed a basal commercial diet without supplementary selenium. In wild species, selenium concentration in the yolk was far higher (4- to 22-fold) than that achieved in the yolk of the domestic chicken consuming a standard basal diet (Pappas et al., 2006c).

References

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