Nutrition and metabolism in poultry: role of lipids in early diet
© Cherian. 2015
Received: 23 February 2015
Accepted: 10 June 2015
Published: 24 June 2015
Modern strains of broiler chickens are selected for fast growth and are marketed anywhere from 36 to 49 days after a 21-day incubational period. For a viable healthy chick, all the necessary nutrients required for growth and development must be provided by the hen through the fertilized egg. The current feeding strategies for improved growth, health and productivity are targeted towards chicks after hatching. Considering the fact that developing chick embryo spends over 30 % of its total life span inside the hatching egg relying on nutrients deposited by the breeder hen, investigations on nutritional needs during pre-hatch period will improve embryonic health, hatchability and chick viability. In this context, investigations on hatching egg lipid quality is of utmost importance because, during incubation, egg fat is the major source of energy and sole source of essential omega-6 (n-6) and omega-3 (n-3) fatty acids to the chick embryo. Due to the unique roles of n-3 and n-6 fatty acids in growth, immune health, and development of central nervous system, this review will focus on the role of early exposure to essential fatty acids through maternal diet and hatching egg and its impact on progeny in meat-type broiler chickens.
KeywordsChick Docosahexaenoic acid Early diet Egg Eicosanoid Embryo Essential fatty acids
Hatching egg: chick’s “early diet”
Breeder hen (maternal) diet and hatching egg lipid components
The physiology of the hen enables egg lipid and fatty acid manipulation within a short duration of time. Upon sexual maturity, hepatic lipogenesis is dramatically enhanced by estrogen in order to meet the demand for vitellogenesis. Yolk fats are synthesized in hen’s liver and are deposited to the yolk through serum via triacylglycerol-rich very low density lipoprotein (VLDL) and phospholipid-rich very high density lipoprotein vitellogenin [3, 4]. VLDL targeted towards yolk is about half the size of normal VLDL and is a specialized form of VLDL that is specific to laying hens called VLDLy . VLDLy forms a complex with the ApoB100 and apovitellenin-1 (apoVLDL-II). ApoVLDL-II bound VLDLy molecules will not be acted upon by lipoprotein lipase (LPL), allowing triglycerides to be deposited to the oocyte intact . No exogenous lipids are transported from the liver to the yolk, only de novo triglycerides are packaged into VLDL for transport. This allows for control over the fatty acid composition of the yolk.
Enriching hatching eggs with essential n-3 and n-6 fatty acids
In chickens, α-linolenic acid (ALA 18:3 n-3) and linoleic acid (18:2 n-6) have to be supplied in the diet and are therefore called essential fatty acids. This essentiality is due to the inability of the hen to insert double bonds (due to the lack of desaturases) beyond δ-9 carbon and can occur only in plants. However, once a double bond is inserted at the 3rd and 6th carbon (from CH3 end locations), the hen can add more double bonds and form longer chain 20 and 22 carbon PUFAs. The process of long chain PUFA synthesis occurs mainly in the liver and includes Δ-6 desaturation, chain elongation and Δ-5 desaturation. Thus the parent ALA is converted to eicosapentaenoic acid (EPA, 20:5 n-3), which is subsequently converted to docosapentaenoic acid (DPA, 22:5 n-3) by chain elongation . The final metabolite, DHA, is synthesized by chain elongation, Δ-6 desaturation, and peroxisomal β-oxidation of DPA . Linoleic acid goes through the same pathway and conversion steps, with arachidonic acid being the major metabolite produced. The efficacy of long chain n-3 PUFA from ALA depends on factors such as concentration of n-6 fatty acids, because same desaturase and elongase enzymes are involved in the synthesis of n-6 and n-3 long chain PUFA. While both n-3 and n-6 PUFA share the same metabolic pathway, each family of fatty acids has been found to exert distinctly different and sometimes opposing biological effects.
Polyunsaturated fatty acid composition of hatching eggs from breeder hens fed diet containing different lipid sources
Fatty acids, %
n-6 fatty acid
Linoleic (18:2 n-6)
Arachidonic (20:4 n-6)
Docosatetraenoic (22:4 n-6)
Docosapentaenoic (22:5 n-6)
n-3 fatty acid
Linolenic (18:3 n-3)
Eicosapentaenoic (20:5 n-3)
Docosapentaenoic (22:5 n-3)
Docosahexaenoic (22:6 n-3)
In ovo nutrition through hatching eggs
In ovo supply of the embryo with vaccines is commonly done in poultry. Recently other substances (e.g., amino acids) injected into the hatching egg to boost metabolism and growth during early post-hatch period has been reported [8, 9]. However, such technology needs special facilities, time and capital to be adopted. Supplying the embryo with nutrients through “maternal” sources (e.g., breeder hen diet and hatching egg) is a natural and sustainable way to approach in ovo feeding. Using this concept, several studies were conducted in our laboratory to assess the impact of early exposure to lipids (e.g., essential fatty acids, conjugated linoleic acid, cholesterol) through hatching egg and its impact on tissue incorporation and fatty acid metabolism during pre and post- hatch period in meat-type broiler chickens [10–12].
In ovo lipid nutrition and fatty acid changes in progeny chicks
Lipids in early diet and its impact on chick tissue fatty acid status during growth
For growth to occur, metabolic precursors must be available to the hatchling. Chicks are precocial and will forage immediately after hatching. However, management practices (e.g., transportation to farms, time gap in hatching window) limit early supply of nutrients to the hatchling through diet. For example, under practical conditions, the newly hatched chick usually does not have access to feed for over 48–72 h post-hatch . Early feed deprivation post-hatch along with the absence of n-3 PUFA in the current commercial hatching eggs may aggravate an n-3 PUFA deficient situation in immune cells and vital organs. Moreover, long-chain n-3 fatty acid in early diet plays crucial roles in immunity in the hatchling . Long chain PUFA such as arachidonic acid and EPA serves as precursors for eicosanoids such as prostaglandins (PG), thromboxanes (TX) and leukotrienes (LT). Eicosanoids are lipid mediators of inflammation. Eicosanoids derived from n-6 fatty acids are more pro-inflammatory than those derived from n-3 fatty acids . Therefore, establishment of a stable and sufficient cell membrane PUFA status during early life is critical for maintaining general metabolism and immune health of progeny chicks.
The impact of early exposure of lipids through hatching eggs on tissue PUFA composition in chicks during post-hatch was assessed. Eggs were produced by feeding breeder hens fish oil as source of n-3 PUFA (n-3 enriched) or sunflower oil as source of n-6 fatty acids (n-3 depleted). The total n-3 fatty acids in n-3 depleted or enriched eggs were 0.9 and 4.1 %, respectively [17, 18]. The chicks hatched from n-3 PUFA enriched or depleted eggs were fed diets lacking in long chain (>20-C) fatty acids (simulating a commercial diet). The fatty acid composition of chick tissues were determined during the grow-out period. The chicks hatched from n-3 fatty acid enriched eggs retained higher levels of EPA, DHA and total n-3 fatty acid in the tissues and cells when faced with an n-3 fatty acid deficient diet during growth. Similarly, the retention of arachidonic acid was higher in liver, heart, brain, spleen, duodenum and cells (thrombocytes, peripheral blood mononuclear [PBMN]) of chicks hatched n-6 PUFA-enriched eggs [17, 18]. The efficacy of the tissues in retaining n-3 or n-6 PUFA varied among tissues and the type of cell membrane. For example, DHA content was higher up to day 14–28 of post-hatch growth in the liver, spleen, bursa and cardiac ventricle of n-3 PUFA-enriched eggs when compared with those of n-3 PUFA depleted eggs . It is clear that early supply of high n-3 fatty acids through egg offer certain advantage for offspring of n-3-enriched eggs, because they had more DHA available at post-hatch, which they obviously used during their first 14–28 days post-hatch. In the duodenum, we noticed that DHA content was highest up to d 14 of growth in chicks hatched from n-3 fatty acid-enriched eggs . A similar impact of egg lipid composition persisting up to 14 days post hatch has been reported in the bone cells in quails .
As acyl moieties of phospholipids in cell membranes, PUFA modulate membrane biogenesis, eicosanoid metabolism, and are essential for the optimal functioning of vital organs. In this context, effectiveness of pre-hatch vs. post-hatch supplementation of n-3 fatty acids in enhancing tissue n-3 fatty acid status in chicks were investigated. Hens were fed a high n-3 (H) or low n-3 (L) diet. Fish oil or sunflower oil was used as source of lipids in H or L diets. Chicks hatched from hens fed the H or L diets were raised on a high (H-H) or no (L-L) n-3 diet. Thus there were 4 treatments (H-H, H-L, L-H, and L-L). In treatments where chicks received H-H diet, brain and hepatic DHA was higher than L-H up to d 20 and d 40 of growth . Similarly, arachidonic acid concentration in brain and liver remained significantly lower in H-H chicks up to day 40 of growth. In conclusion, early supplementation of n-3 PUFA through hen diet and hatching egg has a marked influence of progeny, regardless of post-hatch supply of these fatty acids. These results may have implications in diet of pregnant, or lactating women and the newborn infant. The current intake of omega-3 fats does not meet the recommended intake in this population. Long chain PUFA (especially DHA) is needed for neural growth and development especially during the last trimester of pregnancy and in the first two yr of post-natal life in humans when brain growth and maturation is at its peak [22, 23]. Intense accretion of long chain n-3 PUFA such as DHA has been reported in human brain during the last trimester of pregnancy . A similar pattern of high long chain PUFA accretion during the third trimester of incubation has been reported in studies using avian models [2, 3]. However, differences in nutrient requirements, metabolism, and tissue growth velocity should also be considered before extrapolating results in animal model to humans.
In ovo exposure to n-3 and n-6 fatty acids and its impact on chick brain PUFA status
Chick brain DHA: effect of dietary α-linolenic acid vs. docosahexaenoic acid
In ovo lipid nutrition and impact on mediators of inflammation in progeny chicks
Cell membrane phospholipids are rich in long chain PUFA. Among the different PUFA, ester-linked arachidonic acid and EPA in phospholipids are potentially biologically active precursors and can be mobilized by phospholipase A2 to generate the free arachidonic and EPA which then can act as substrates for cyclooxygenase or lipoxygenase which produces eicosanoids. Eicosanoids derived from arachidonic acid such as LTB4, PG2, and TX2 are pro-inflammatory, and eicosanoids derived from EPA (e.g., LTB5, PG3,TX3) are less inflammatory . To investigate whether tissue n-3 or n-6 PUFA status affects eicosanoid production, cells or tissues were taken at day of hatch, 7, 14 and 21 from chicks hatched from n-3 enriched or depleted eggs. It was observed that on the day of hatch, chicks from n-3 PUFA enriched eggs had the lowest liver and serum interleukin (IL-6), cardiac PGE2, TXA2 concentrations upon exvivo challenge [20, 10]. The effect of maternal diet persisted up to day 7 in the cardiac tissue eicosanoid concentrations (17). Similarly, LTB4 production by thrombocytes from n-3 depleted chicks was greater than those chicks hatched from n-3 enriched eggs . The significant difference in LTB4 production in progeny birds persisted up to 21 day of bird growth. In addition, the ratio of LTB5 to LTB4 concentrations was higher in chicks hatched from n-3 PUFA enriched eggs. The ratio of LTB5 to LTB4 was significantly correlated to the ratio of EPA to arachidonic acid in spleen and bursa in these chicks. These results indicate that an integral relationship exists between early dietary exposure to n-3 or n-6 PUFA through egg on tissue/cell fatty acid content, and consequently production of inflammatory mediators in progeny chickens.
In ovo lipid nutrition: impact on immune responses in progeny chicks
Inflammation is part of the chick’s immediate response to challenges (e.g., infection) and is part of the normal innate immune responses. However, when inflammation occurs in an uncontrolled or inappropriate manner, it can affect production performance or disease progression. In chicks, developmental events important for immuno-competence are initiated during the embryonic period and continue in the early weeks following hatching . Therefore, targeting towards a robust immune system during early post-hatch may enhance chick quality and health. Hatching through first week of life is the most vulnerable period affecting early mortality and culls. During this time, the chick faces abrupt and profound metabolic, physiological and environmental stressors. These peri- and early post-hatch stressors in chicks are contributed through: shifting from chorio-allantoic respiration to pulmonary respiration with resulting exposure to atmospheric oxygen and increase in rate of oxidative metabolism; transition from yolk lipid-based metabolism to solid carbohydrate-based metabolism through the diet; the long gap in hatching time (>24 h), delays in shipments to farms leading to early starvation. In addition, other parental factors such as breeder hen age and nutrition and environmental conditions of the farm can affect health and quality of the newly hatched chick [2, 3]. Chick quality and survivability during early post hatch period depend upon their ability to respond effectively, appropriately and timely to these different stressors.
Summary of studies investigating the effect of early exposure of lipids and its impact on progeny chickens immune or inflammatory responses
Lipids in maternal diet
Reported findings in the progeny during growth
Bullock et al., 2014 
Fish oil vs. sunflower
Chicks from fish oil-fed hens had the lower liver and serum IL-6 concentrations than those from sunflower-oil fed hens.
Gonzalez et al., 2011 
Fish oil vs. sunflower
Early access to n-3 PUFA increased the expression of COX-2: actin ratio in lipopolysaccharide injected birds.
Sunflower vs. Fish oil
Prostaglandin E2 concentration in cardiac tissue was higher in one day-old chicks from hens fed sunflower oil than those from fish oil.
Cherian et al. 2009 
Sunflower vs. Fish oil
Prostaglandin E3 and thromboxane A2 production by peripheral blood mononuclear cells was reduced in 7-day old chicks from hens fed low n-3 (0 % DHA) vs. high n-3 (4.2 % DHA).
Hall et al., 2007 
Sunflower vs. Fish oil
Ratio of LTB5 to LTB4 remained higher up to day 21 in chicks hatched from high omega-3 (4.1 %) vs. low omega-3 (0.9 %) eggs.
Wang et al. 2002, 2004 
Sunflower and Linseed oil
High linoleic:ALA (12.4:1 vs. 0.8:1) led to lower BSA-specific IgG titer in the serum in the hatchlings Feeding breeder hens 5 % fish oil diet decreased BSA-induced wing web swellings at 4 week of age in chicks.
Chicks from the hens fed linseed and fish oil diet had lower splenocyte and thymus lymphocyte proliferative response than those from sunflower-oil fed chicks.
Liu and Denbow 2001 
Soybean oil, Chicken fat, Menhaden oil
Maternal dietary n-3 fatty acids lowered the ex vivo prostaglandin E2 production of tibiae in newly hatched quail compared to those from hens fed soybean oil or poultry fat.
In ovo lipid nutrition: impact on hatchling antioxidant status
Modern strains of birds selected for fast growth have high metabolic rates and increased oxidative stress. Antioxidant capability at hatching time is considered to be an important determinant of chick viability. Antioxidants in the animal body work together as the so called “antioxidant system” to prevent damaging effects of free radicals and toxic products of their metabolism. The chick’s antioxidant system includes enzymes (e.g., superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase) and molecules (e.g., glutathione, vitamin A and E, and carotenoids) [30, 31]. Antioxidants are needed to protect chicks from oxidative damage. Chick nutritional encephalomalacia is a classical vitamin E-deficiency syndrome characterized by a severe hemorrhagic lesion of the cerebellum resulting in ataxia and death . Experimental induction of nutritional encephalomalacia in chicks fed high PUFA diet attests to the unique need of antioxidants such as vitamin E in providing protection against oxidative damage . Hatching time is considered to be a period of high oxidative stress due to long-chain PUFA accretion in tissues, exposure to atmospheric oxygen, onset of pulmonary respiration, and sudden increase in rate of oxidative metabolism  and the hatchlings are expected to react with a compensatory induction of endogenous antioxidants. The impact of hatching egg n-3 PUFA content on antioxidant status was assessed. It was observed that chicks hatched from hens fed fish oil had the lowest level of liver vitamin E content compared to flax or sunflower oil . Liver tissue super oxide dismutase and glutathione peroxidase activity were highest in chicks hatched from hens fed fish oil [34, 35]. These results suggest that regulation of antioxidant activity in newly hatched chicks are dependent on parent hen diets and egg PUFA composition.
Overall effects of early exposure of omega-3 lipids through hatching egg in progeny chicks
• Increase in tissue cell membrane n-3 fatty acids
• Increase in production of less pro-inflammatory eicosanoids
• Decrease in long chain n-6 PUFA in cell membrane phospholipids
• Decrease in production of pro-inflammatory eicosanoids
• Decrease in production of interleukin-6
• Decrease in cell mediated immune response measured through DTH response
• Reduced splenocyte and thymus lymphocyte proliferative response
• Reduction in hatched chick body weight
• Reduction in hepatic tocopherol content
• Increase in liver tissue SOD and GSH-PX activity
• Alteration in the expression of inflammatory COX-2 proteins
• Alteration in the expression of genes related to lipid metabolism
Polyunsaturated fatty acid
Yolk sac membrane
Very low density lipoprotein
Delayed type hypersensitivity
Peripheral Blood Mononuclear
Author acknowledges the National Research Initiative of the USDA Cooperative State Research, Education and Extension Service, grant number 2004-35204-14654, Oregon State University Experiment Station Hatch fund, Oregon State University Animal Health Fund, and Walther H. Ott Professorship in Poultry Science awarded to G. Cherian.
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