Nutritional Imprinting of Young Broilers
By Roselina Angel
Features Business & Policy TradeStudies in the US indicate that you can teach young broiler chicks new tricks when it comes to feed
Young broiler genes, if taught early enough, will learn more efficient
utilization of feed according to a paper presented by Roselina Angel of
the University of Maryland and Chris Ashwell of North Carolina State
University at the Midwest Poultry Conference in St. Paul, Minnesota, in
March.
Young broiler genes, if taught early enough, will learn more efficient utilization of feed according to a paper presented by Roselina Angel of the University of Maryland and Chris Ashwell of North Carolina State University at the Midwest Poultry Conference in St. Paul, Minnesota, in March.
‘Learned’ Efficiency. New studies demonstrate that young broiler genes can quickly learn to be more efficient in their use of nitrogen (N) and phosphorus (P) by employing nutritional imprinting. Advertisement
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The new studies demonstrate that young broiler genes can quickly learn to be more efficient in their use of nitrogen (N) and phosphorus (P) and that nutritional imprinting can be a potent management and nutritional tool. It can give the birds the long-term ability to more efficiently utilize what would usually be considered deficient concentrations of dietary P and protein when these are fed in the finisher and withdrawal phases.
While additional study is required the result could be one of the most efficient and possibly the most economical method of controlling NH3 production from poultry facilities. In general, N excretion is directly related to the animal’s N (protein) intake and its growth rate that is related to the amount of N retained by the body. Numerous nutritional studies have demonstrated that dietary manipulation in monogastric animals can be a useful tool to reduce NH3 emissions. Several nutritional strategies have been developed to reduce N concentrations in poultry excreta and consequently reduce atmospheric NH3 emissions.
Some of these strategies include reducing dietary protein concentrations while providing adequate essential and some non-essential amino acids at the correct balance in the diet by supplementation with synthetic amino acids, minimizing feed and water waste, separate sex and phase feeding, enzyme supplementation, and minimizing feed nutrient variability.
Most of the strategies mentioned partially address environmental concerns as well as production cost challenges related to diet P and protein. Most of these strategies have proven effective to varying degrees but they have the potential to increase cost and increase risk by increasing the possibilities of lower productivity in the field and at processing.
An alternative is epigenetic regulation of gene expression by early nutritional imprinting that results in changes in genes of significant economic importance to the poultry industry. These gene modifications brought about by an early-life dietary change need to be long lasting such that once the early nutritional modification is replaced with adequate or deficient feeds, the ability of the animal to better utilize specific nutrients is maintained.
Background on Epigenetic Regulation
Observations have been made where conditioning chickens in early-life imparts long-term effects. One such report looked at temperature or thermal stress. The goal for these studies was to identify a mechanism to impart tolerance to acute heat stress in chickens. It was found that high temperatures during the first week of life modulated the response to thermal stress later in life. By simply increasing the brooding temperature from 30 C to 37.5 C for 24 hours within the first five days post-hatch, birds are able to tolerate six hours of exposure to 35 C at 42 days of age, while “unconditioned” birds are unable to acclimate. The mechanism for this conditioned response is unknown. Several studies speculate that it is during the period immediately post hatch (neonatal) that the chick is developing the connections in the brain for the detection and regulation of body temperature.
Early dietary adaptation
Adaptation to low nutrient diets has been long recognized. Animals respond to nutrient restriction in general by increasing absorption rates and utilization efficiency, which decreases excretion of the restricted nutrients.
Adaptation to P and Ca restricted diets has been previously reported in chickens. By comparing the duodenal calbindin concentration and its changing pattern with age for 1991 and 2001 strains of broilers, a 2003 British study concluded that modern broilers exhibit higher capacity of adaptation to P or Ca deficiency and this capacity remains high for the whole growth period.
Although several reports demonstrate the ability to program chicks through early dietary manipulation to improve Ca and P utilization later on in life, there has been little work applying this concept with dietary protein utilization. The lysine requirement for broiler chickens has been studied extensively, and recommendations have been made for different growth phases. Lysine is often considered first co-limiting amino acid with methionine in broiler diets, and is added in synthetic form to meet the bird’s requirement. The interaction between protein and lysine is considered an important factor that affects broiler performance and carcass quality.
Early Nutrient Imprinting
No literature could be found on work conducted to evaluate the long-term effects of early P or Ca restriction on growth performance, bone mineralization, and P absorption in later growth phases in poultry. Thus, the authors proceeded to investigate if birds had the capacity to adapt to low P diets. The application of the adaptation principle in poultry may allow for decreasing both diet and excreted P without sacrificing performance and provide an additional low cost tool to decrease P in poultry litter.
The goal of this work was to determine if adaptation occurred in broilers and then to try to identify the mechanisms of this adaptation. The authors evaluated the ability of the chicken to adapt to a moderate early life deficiency in P and Ca and characterized this adaptation by examining the impact of the previous P and Ca status (starter phase, hatch to 18 d) on performance, bone characteristics, and nutrient absorption of broilers in the grower phase (19 to 32 d).
Briefly, broilers fed a diet moderately deficient in P and Ca from hatch to 18 d demonstrated the ability to adapt to the deficiency. This was shown in the increased total P and Ca ileal absorption (Table 1), the increased PP disappearance, improved growth, and improvement in bone measures including tibia ash, tibia and shank bone mineral density and bone mineral content in a later growth phase (18 to 32 d). The data indicate that in birds during the period immediately post hatch there is a phenomenon occurring that permanently alters the birds’ response to its environment.
This adaptation or conditioning, whichever term you choose to use, is a real observable fact for which no underlying mechanism has been previously proposed.
It has been proposed that adverse nutritional conditions during fetal development lead to adaptive changes in metabolism that lead to a “thrifty phenotype” in the offspring. Photo by Frank Robinson |
A second experiment was done to determine the effects of diet P on performance and expression of the chicken intestinal NaPcoT. Experimental diets were formulated to be adequate (control diet (C) consisting of 1.11% Ca and 0.50% available P (NRC levels)) or deficient in P (restricted diet (L) containing 0.59% Ca and 0.25% available P) and fed to Ross 308 chicks from hatch to four days of age (90 hour). All birds were then fed a control diet (C) consisting of NRC recommended levels of Ca and P until day 22. From day 22 to 38 the birds were either maintained on a C diet at NRC levels of Ca and P (0.7% and 0.3% respectively) or an L diet (0.4% Ca and 0.12% P).
The three dietary treatments, C-C-C, C-C-L, and L-C-L met all other NRC (1994) nutrient recommendations. Performance data were collected for each dietary phase including weight gain, feed conversion, bone ash, and apparent ileal Ca and P retention.
Broilers fed the moderately deficient diet (L) for 90 hours post hatch were better able to handle a deficiency in P in the grower/finisher phase (22 to 38 d of age) than those fed a control diet in the first 90 hours. Not only were the broilers fed the L diet early on heavier at 38 days of age, but they were more efficient in converting feed to gain, and had higher tibia ash and higher P retention than those fed the C diet in the first 90 hr of life. This clearly establishes that “imprinting” or modifications are occurring in the animal that are long term and that allow for improved P utilization when P deficient diets are fed in the grower/finisher phases.
Based on the controlled battery work done to date it appears that nutritional imprinting can be a potent management and nutritional tool that imparts on the birds the long-term ability to more efficiently utilize deficient concentrations of dietary P and protein when these are fed in the finisher and withdrawal phases. More work is needed to determine how well the P imprinting concept works in floor pens and under conditions more similar to those seen in industry and to further explore the initial finding with high lysine in starter diets.
The full report (in PDF format) with references is available at www.canadianpoultrymagazine.com .
Epigenetic Regulation The growing incidence of metabolic diseases in humans, such as obesity, diabetes, and cardiovascular disease has sparked interest and research efforts into both their genetic and environmental (nutritional) basis. The maternal diet, and therefore the nutrient supply to the developing oocyte, embryo or fetus, is one of the principal environmental factors influencing the development of the offspring. A reliable and balanced supply of amino acids, lipids and carbohydrates is required to support the high rates of cell proliferation and the key developmental processes that take place during fetal development. Eukaryotic cells have evolved a complex series of nutrient sensors that are able to regulate gene expression in response to imbalances in the supply of nutrients. In adults these systems serve two purposes; first to protect the cell from damage caused by acute deficiencies and second to optimize homeostatic control to deal with a prolonged excess or deficiency of a particular nutrient. This second process may have a critical impact on the long-term health of the offspring. It has been proposed that adverse nutritional conditions during fetal development lead to adaptive changes in metabolism that lead to a ‘thrifty phenotype’ in the offspring. Poor nutrition in early life produces permanent changes in glucose-insulin metabolism, including a reduced capacity for insulin secretion and insulin resistance. However, if this ‘programming’ of metabolism during embryonic and fetal development is inappropriate for the long term nutritional environment where the animal will live in it may lead to adverse long-term consequences. The initiating factor(s) for fetal programming may be nutrient(s) interacting directly with genes and their regulatory elements at the cellular level, altering patterns of growth and gene expression. It is becoming apparent that embryonic and fetal cells have a complex system that integrates nutritional signals coming from their environment with development such that survival is ensured. The full impact of inappropriate programming of metabolic regulation is only just beginning to be appreciated. The available evidence suggests that nutrient sensing regulatory systems are present in many critical tissues during early development. Similar observations to those found in mammals have been made in the chicken where conditioning in early-life imparts long-term effects of temperature or thermal stress. |
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