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METABOLISM AND NUTRITION |
* University of Arkansas, Center of Excellence for Poultry Science, Fayetteville 72701; and Growth Biology Laboratory, USDA-ARS, 10200 Baltimore Ave., Beltsville, MD 20705
1 Corresponding author: ccoon{at}uark.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Key Words: breeder • feeding regimen • metabolic hormone
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Although differences between restricted- and ad libitum-fed birds have received much attention, the endocrine response to specific types of feed-restriction programs is not well documented. Both ED and SKIP programs result in periods when the bird is without feed. However, the length of the fasting period differs between the 2 programs. Fasting is known to influence many metabolic processes. In simple terms, a shift is made from anabolism to catabolism and from lipogenesis to lipolysis (Buyse et al., 2000). In chickens, fasting reduces circulating 3,3',5-triiodothyronine (T3), insulin, and insulin-like growth factor-I (IGF-I) levels (Decuypere and Kuhn, 1984), whereas plasma glucocorticoid levels, insulin-like growth factor-II (IGF-II; Kita et al., 2002), and growth hormone are increased (Buyse et al., 2000). Plasma corticosterone has been shown to increase during periods of stress in the chicken (Nir et al., 1975) and, in particular, during stress associated with feed restriction (Weber et al., 1990; Latshaw 1991). Several authors have shown that practical levels of feed restriction can lead to chronic stress in broiler breeders (Hocking et al., 1996; De Jong et al., 2002). Relationships have been identified between metabolic hormone levels and expression of several lipogenic genes (Richards et al., 2003). Understanding the potential effects of ED or SKIP feeding on metabolic hormones and metabolites may provide insight into the long-term effects of such feeding programs.
This study aimed to determine the effects of feeding regimens on plasma hormone profiles and metabolites. Furthermore, this study intended to characterize the changes in these parameters over time after feeding. A better understanding of the metabolic responses to feed restriction may be of help in developing the most effective feeding regimens to enhance reproductive efficiency in broiler breeders.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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A flock of 350 Cobb 500 pullets was raised in 10 floor pens (35 birds per pen) from 1 d old. The Cobb Breeder Management Guide (Cobb-Vantress, 2005) was used as a reference for all management conditions, including light schedules for dark-out rearing houses. The compositions of the diets used throughout the experiment are shown in Table 1
. The starter diet was fed from 0 to 4 wk of age and the grower diet was fed from 4 wk until the end of the experiment.
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Diets were offered to all birds for ad libitum consumption for the first 2 wk. From 2 to 4 wk, all birds were fed restricted amounts of feed every day. At 4 wk of age, feed-restriction treatments were implemented. Half of the birds (5 randomly selected pens of 35 birds each) were fed restricted amounts of feed every day (ED) from 4 to 16 wk of age. Feed allocation was based on breeder recommended guidelines to reach target BW. The other half of the birds were fed every other day (SKIP). Total feed allocation did not differ between the 2 treatments. For example, if the ED group received 50 g per bird per day, the SKIP group would receive 100 g per bird every other day. Birds were weighed weekly in groups to adjust feed allocation to ensure that target BW was met.
At 108 d of age, 52 pullets from the ED group and 76 pullets from the SKIP group were randomly selected and individually caged. Cages were each equipped with an individual feeder and a water trough. Birds were fed individually and provided with free access to water at all times. During the acclimation period, the ED- and SKIP-feeding regimens continued. The photoperiod was 8L:16D at this time. After 4 d of acclimation to individual cages, at 112 d, the 52 pullets from the ED group were fed 74 g of standard breeder grower diet (Table 1
), and the 76 pullets from the SKIP group were fed 148 g of the same diet at 0700 h. Blood samples were collected from 4 pullets from each feeding regimen immediately prior to feeding and then at intervals after feeding. The sampling intervals were 15 min, 30 min, 45 min, 60 min, 90 min, 2 h, and 4 h after feeding and then every 4 h up to 24 h for ED pullets and 48 h for SKIP pullets. These times represent a full feeding cycle for each group. Blood samples (5 mL) were collected from each bird by cardiac puncture using EDTA as anticoagulant. The blood samples were centrifuged in a TJ-6 centrifuge (Beckman Coulter Inc., Fullerton, CA) for 10 min at a relative centrifugal force of 1,000 x g, and plasma was stored at –20 C for further analysis of leptin, glucagon, insulin, T3, thyroxine (T4), IGF-I, IGF-II, and corticosterone.
Feed Retention in Crop
A further 32 ED-fed and 48 SKIP-fed pullets were individually caged at 112 d. A meal of 74 g was fed to ED pullets and a meal of 148 g was fed to SKIP pullets. At 4-h intervals after feeding, 4 pullets from each treatment were euthanized by CO2 asphyxiation and all crop contents were removed and weighed. A homogeneous sample of the removed crop contents was dried and weighed. The sample DM percentage was used to determine the total dry feed content in the crop at each sampling interval.
Plasma Hormones
Specific RIA were used to determine plasma hormone concentrations. All samples were analyzed within 1 assay to avoid interassay variations. Double-antibody RIA were used to determine plasma concentrations of IGF-I with an intraassay CV of 2.8% (McMurtry et al., 1994), chicken IGF-II with an intraassay CV of 3.7% (McMurtry et al., 1998), insulin with an intraassay CV of 2.2% (McMurtry et al., 1983), and leptin with an intraassay CV of 3.9% (Evock-Clover et al., 2002). Triiodothyronine and T4 were determined as previously described (McMurtry et al., 1988) and had intraassay CV of 2.5 and 2.8%, respectively. Plasma glucagon (Linco Research Inc., St. Charles, MO) was determined as described by McMurtry et al. (1996) with a commercial kit and had an intraassay CV of 1.9%. For glucagon analysis, an aliquot of plasma was stored in the presence of 1,000 kIU of aprotinin. Aprotinin is a protease inhibitor that is used to prevent the degradation of glucagon. Plasma corticosterone was determined as described by McMurtry et al. (1991) with a purchased kit (ICN Pharmaceuticals, Costa Mesa, CA). The intraassay CV for this assay was calculated as 1.6%.
Plasma Metabolites
After hormone assays were complete, remaining plasma samples were analyzed for the following plasma metabolites: glucose (kit number GAHK20-1KT for glucose, and kit number TR0100-1KT for triglycerides, Sigma-Aldrich, St. Louis, MO), nonesterified fatty acids (NEFA; kit number 994-75409, Wako Chemicals USA, Richmond, VA), uric acid (kit numbers U582-480 and U580-400, Teco Diagnostics, Anaheim, CA), and triglycerides (Sigma-Aldrich).
Statistical Analyses
Data analysis was performed by using JMP IN 5.1 (SAS Institute Inc., Cary, NC) statistical analysis software. Data were analyzed by ANOVA. The statistical model included terms for feeding regimen and time after feeding. Data are presented as mean ± SEM. When effects were significant, means were separated by Tukey’s Studentized range test (Tukey, 1991). All statements of significance are based on testing at P 
0.05.
Animal Use
All procedures were carried out in accordance with Animal Use Protocol No. 03008 for the experiment, which was approved by the University of Arkansas Institutional Animal Care and Use Committee.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Data presented in Figure 1 indicate that there was an initial period of quick reduction in crop contents, which slowed after approximately 6 to 8 h in both ED and SKIP pullets. For ED-fed pullets, the crop had emptied by approximately 12 h after feeding. The crop of SKIP-fed pullets had emptied by 24 h after feeding. The overall rates of crop emptying in the ED and SKIP birds were very similar. However, because of the larger amount of feed offered to SKIP birds, their crops contained more (P 0.05) feed at each comparable time point.
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Mean plasma hormone and metabolite values over the entire experimental period are presented in Table 2. Mean IGF-I and leptin concentrations were higher (P 0.05) in ED than in SKIP birds. Mean corticosterone levels were higher (P 0.05) in SKIP birds than in ED birds.
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) did not differ (P 0.05) between ED and SKIP birds prior to feeding. Insulin levels increased (P 0.05) after feeding in both ED and SKIP birds. The plasma insulin level of SKIP birds was between 2- and 3-fold greater than that for ED birds for the first hour after feeding. After approximately 4 h, the insulin levels of ED and SKIP birds did not differ. Prefeeding levels were restored by 2 h after feeding in ED birds and by 4 h in SKIP birds. Plasma insulin reached a minimum at approximately 12 h after feeding in ED birds and approximately 28 to 32 h in SKIP birds.
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) did not differ (P 0.05) between ED- and SKIP-fed pullets immediately prior to feeding. Glucagon levels decreased (P 0.05) immediately after feeding in both treatments. Glucagon levels remained similarly low in both treatments in the first 8 h after feeding. Glucagon was elevated (P 0.05) in ED birds from 12 to 16 h after feeding. This coincided with the time of crop emptying. Glucagon levels were first elevated (P 0.05) after 28 h in the SKIP birds. This also coincided with the time of crop emptying in these birds. Interestingly, there was a drop in glucagon in the ED birds from 16 to 20 h. Although this drop in glucagon was nonsignificant, it was matched by a significant (P 0.05) drop in glucagon from 36 to 44 h in SKIP birds. Closer inspection of the insulin levels (Figure 2) of each group showed that insulin levels were nonsignificantly elevated in both ED- and SKIP-fed birds at the times these drops in glucagon were noted.
Levels of IGF-I were elevated in ED birds after 15 and 30 min (Figure 2) but returned to prefeeding levels by 45 min. No increase was seen in IGF-I after feeding SKIP birds. In fact, IGF-I decreased in the first 15 min after feeding. The minimum IGF-I level was observed at 2 h after feeding in SKIP birds. Levels of IGF-II (Figure 2) were briefly elevated after feeding ED birds, but by 1 h after feeding, IGF-II had reached levels significantly lower than those at 0 h. In the SKIP birds, IGF-II decreased after feeding and reached minimum levels during the early part of the off feed day (24 to 28 h). The IGF-II began to increase between 12 and 16 h in ED birds and at 32 to 36 h in SKIP birds. Much like IGF-I, there was an elevation in IGF-II in SKIP birds during the second dark period after feeding.
Levels of T3 increased after feeding in both treatments (Figure 3). Levels were significantly (P 0.05) higher than prefeeding levels by 90 min after feeding for both ED- and SKIP-fed pullets. Maximum T3 levels were reached at 8 h after feeding for both groups. The maximum level of T3 did not differ (P 0.05) between treatments. After the peak was reached, T3 declined more rapidly in ED-fed birds, and by 12 h, T3 was lower in ED- than in SKIP-fed birds. Prefeeding levels were restored by 20 h in ED birds, whereas it took 32 h for the same to happen in SKIP birds. Plasma T4 levels increased above prefeeding levels by 2 h postfeeding and then declined steadily until a minimum was reached at 12 h in ED birds (Figure 3). In SKIP birds, plasma T4 was elevated above prefeeding levels within 1 h after feeding. Subsequently, T4 levels declined until a minimum was reached at 8 h after feeding.
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) decreased (P 0.05) within 30 min after feeding in ED birds. In contrast, the highest levels of corticosterone in SKIP birds were observed at 30 min after feeding but returned to lower levels very rapidly. In ED-fed birds, the maximum corticosterone level was observed at 8 h. In SKIP-fed birds, a second increase in corticosterone was observed at 20 h, followed by a decline to 28 h and a steady increase to 48 h thereafter.
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0.05) than pre-feeding levels within 30 min after feeding in both groups (Figure 5). After 30 min, leptin levels began to increase in both groups. The pattern of fluctuations in leptin concentration was very similar in both groups. Although leptin levels were higher (P 0.05) in ED birds at every time point measured, the changes in leptin concentration in ED birds were paralleled by those in the SKIP birds.
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Plasma glucose concentration immediately prior to feeding was lower (P 0.05) in SKIP than in ED birds (Figure 6). Plasma glucose increased immediately after a meal in both ED and SKIP birds. There was a general decline in plasma glucose levels after 30 min, including a marked decrease at 45 min in both ED and SKIP birds. Prefeeding glucose levels were restored by 2 h in ED birds. A secondary spike in glucose concentration was observed in both sets of birds. In ED birds, an increase in glucose was seen at 12 h. Although the 12-h level was not significantly higher than the 8-h level, it did coincide with the increase in insulin and decrease in glucagon noted earlier. In SKIP birds, an increase (P 0.05) in glucose was noted at 28 h. Again, this increase coincided with previously mentioned increases in insulin and decreases in glucagon at the same time point.
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0.05) in NEFA concentration in both ED- and SKIP-fed birds (Figure 6). There was a significant (P 0.05) increase in NEFA levels from 8 to 12 h in ED birds and from 32 to 36 h in SKIP birds. The maximum NEFA levels were observed at 24 h in ED birds and at 40 h in SKIP birds.
Plasma triglyceride levels (Figure 6) increased after feeding in both ED- and SKIP-fed birds. The increase in triglycerides in ED birds continued until a maximum was reached at 2 h after feeding. After 2 h, triglyceride levels remained relatively constant until a sharp decline (P 0.05) was noted from 12 to 16 h. By 20 h, prefeeding triglyceride levels had been restored. The maximum triglyceride levels were reached by 8 h in SKIP birds, followed by relatively constant levels until a sharp decline (P 0.05) was noted from 28 to 32 h. By 36 h, prefeeding levels had been restored.
Uric acid levels increased after feeding in both ED and SKIP birds, but began to decline again by 1 h in SKIP birds and by 90 min in ED birds (Figure 6). However, a second increase (P 0.05) in plasma uric acid levels was noted for ED birds from 4 to 12 h. In SKIP birds, there was also a second increase (P 0.05) in uric acid from 20 h to 28 h, followed by a general decline from 28 to 48 h.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Once the crop emptied, the physiological responses associated with fasting became apparent. In simple terms, a shift was made from anabolism to catabolism and from lipogenesis to lipolysis (Buyse et al., 2000). Bennett et al. (1990) conducted an experiment very similar to the one reported here, in which they measured heat production and the respiratory quotient (RQ) of 16-wk-old breeder pullets fed ED or SKIP. They followed these parameters over a 48-h period. They fed the ED birds a 74-g meal and the SKIP birds a 148-g meal, which matched the feeding levels in this study. They showed that, on average, SKIP-fed birds produced more heat per kilogram of BW than ED-fed birds. The reported inefficiency in feed utilization of SKIP birds compared with ED birds (Leeson and Summers, 1985; Bennett and Leeson, 1989; Katanbaf et al., 1989a) is supported by this observation. Bennett et al. (1990) were also able to show, by means of RQ values, that SKIP-fed birds were in an absorptive state during feeding days, but that they were mobilizing nutrients (fat and protein) from body reserves during the off-feed days. The changes in substrate utilization indicated by RQ values in their study coincide well with the times we noted for crop emptying in both ED- and SKIP-fed birds. For example, they showed that RQ declined sharply from approximately 1.0 at 24 h after feeding to approximately 0.7 by 32 h after feeding in SKIP birds, indicating the utilization of fat and protein at this time. The RQ values noted for ED birds ranged from 0.80 to 0.91, whereas those for the SKIP birds ranged from 0.67 to 1.05. They attributed this larger range in SKIP-fed birds to the obvious fluctuations in feed supply, whereas the more constant feed supply for ED-fed birds meant they were able, in large part, to avoid amino acid breakdown for gluconeogenesis.
Insulin levels were not dramatically affected during fasting in either ED or SKIP birds. In SKIP birds, however, the increase in insulin secretion in response to feeding was greater than that noted for ED. Regulation of insulin release is mediated by cholecystokinin, glucagon, and absorbed amino acids in birds. The effects of blood glucose on insulin release are less significant in birds than in mammals. Glucagon levels did not differ in ED and SKIP birds before feeding or in the immediate post-feeding period. In ED birds, increased glucagon levels were observed 12 h after feeding. This coincided with the time of crop emptying. In SKIP birds, elevated glucagon levels were observed by 24 h, which also coincided with the time of crop emptying. The physiological response to fasting occurred once the crop emptied.
Of great interest in this study were the coordinated fluctuations in insulin and glucagon that occurred at approximately 20 h after feeding in ED birds and 40 h after feeding in SKIP birds. In both cases, glucagon levels were decreased and insulin levels were marginally increased. Although the changes in insulin levels were nonsignificant, their apparent coordination with significant decreases in glucagon suggests that genuine changes did in fact occur. Analysis of blood glucose levels indicated secondary spikes at 12 h after feeding in ED birds and 28 h after feeding in SKIP birds. Fasting blood glucose levels were higher in ED than SKIP birds but mean glucose levels over the 48-h period did not differ. The cause of these observations is not clear. It is possible that when the postabsorptive state is reached, elevated glucagon activates glycogen phosphorylase in the liver and gluconeogenic enzymes in the liver and muscle, resulting in a period of hyperglycemia. This in turn decreases circulating glucagon and causes relatively small increases in circulating insulin. This speculation is supported by the observations of Hazelwood (2000), who postulated a similar sequence of events.
Levels of IGF-I and IGF-II are regulated by nutritional state (for a review, see Thissen et al., 1994). In the study reported here, overall IGF-I levels were higher in ED than in SKIP birds, whereas overall IGF-II levels did not differ. Although overall mean IGF-II levels did not differ, levels were consistently higher in SKIP birds than in ED birds from 1 to 12 h after feeding and were elevated in both ED and SKIP birds late in the fasting period. Other authors have presented comparable findings. For example, Buyse et al. (2002) and Kita et al. (2002) demonstrated that plasma IGF-I levels were lower in fasted birds than in ad libitum-fed birds, whereas IGF-II levels were higher in fasted birds. Hepatic IGF-I mRNA expression is also lower in fasted birds (Kita et al., 2002). In addition, Kita et al. (1996) showed that liver IGF-I mRNA levels changed in parallel with changes in plasma IGF-I. A low-protein diet resulted in similar effects on fasting (Rosebrough and McMurtry, 2000). Despite overall feed intakes being identical, these feeding regimens were clearly able to regulate plasma IGF-I levels. It is possible (Buyse et al., 2000) that factors such as insulin and T3 may regulate acute IGF-I release after refeeding. Kita et al. (1996) showed that plasma IGF-I increased with increasing dietary protein from a deficiency to the requirement, and that above those levels it decreased significantly. Refeeding fasted birds with a low-protein diet depressed IGF-I production after refeeding (Rosebrough and McMurtry, 2000). In this study, both ED and SKIP birds had elevated IGF-II levels during the latter stages of their fasting periods. Upon refeeding, these levels decreased very gradually.
Plasma T3 followed a very similar pattern in ED and SKIP birds, but the overall mean was higher in SKIP birds. The relevance of T3 levels to the level of lipogenesis has been demonstrated by other authors. Increased lipogenesis in previously fasted, refed chickens can be ascribed, in part, to increased circulating T3 levels (Hillgartner et al., 1996; Rosebrough, 2000; Richards et al., 2003). Acetyl-coenzyme A carboxylase catalyzes the rate-limiting step in lipogenesis. Hillgartner et al. (1996) also showed that transcriptional control of acetyl-coenzyme A carboxylase mRNA levels was mediated in part by T3, along with insulin, glucagon, and glucose. Triiodothyronine also induces sterol regulatory element-binding protein-1, which is a key transcription factor controlling expression of several lipogenic genes (Richards et al., 2003). Rosebrough and McMurtry (2000) concluded that feeding regimens could regulate the conversion of T4 to T3. Conversion of T4 to T3 is an important part of thyroid function and allows thyroid hormones to exert their full biological activity, because thyroid hormone receptors preferentially bind T3. Thyroxine can be deiodinated in the outer ring to form the more active T3. Type I deiodinase (D1) is the enzyme involved, and it catalyzes an outer ring deiodination. Outer ring deiodination of T4 is the only way to produce active T3. Feed restriction does not markedly affect levels of in vitro hepatic D1 activity (Darras et al., 1995). It is possible that the lack of cofactors for D1 activity during starvation may reduce D1 activity in vivo, which may explain the lower levels of T3 observed during fasting. The increase in T3 after refeeding (Swennen et al., 2005) is likely the result of reduced type III deiodinase activity in the liver (reduced T3 degradation), rather than a result of increased conversion of T4 to T3. This suggestion is supported by Buyse et al. (2000), who found that T4 and D1 were not significantly changed after refeeding.
In our study, the overall mean corticosterone level was 2-fold higher in SKIP birds compared with ED birds. Two significant peaks were noted in corticosterone levels in SKIP birds. One was seen immediately after feeding, suggesting that there was elevated stress at this time in SKIP birds. Under conditions of feed restriction, competition for feed is intense and aggressive feeding behavior is common. The second peak in corticosterone concentration was observed at 20 h after feeding, after which levels remained elevated until 48 h. Elevations in corticosterone of smaller magnitude were noted at 8 h in ED-fed birds. In both ED and SKIP birds, corticosterone was elevated at the last time point observed before crop emptying. This finding confirms the relationship between hunger, stress, and plasma corticosterone.
Corticosterone, apart from being an indicator of stress, can have various metabolic effects in chickens. For example, it increases glucose production in the liver (Amatruda et al., 1985) while reducing insulin-mediated uptake and utilization of glucose in adipose tissue and muscle (Olefsky, 1975) and enhancing proteolytic activity of the muscle. Lipolysis is also promoted by activation of the cyclic adenosine monophosphate-dependent hormone-sensitive lipoprotein lipase (Cahill, 1971). These actions are attributed partly to a direct effect of corticosterone and partly to the impairment of insulin signaling, or insulin resistance (Saad et al., 1993). In our study, the insulin response to feeding in SKIP birds was far greater than that observed in ED birds.
The action of insulin is mediated through a cascade of events initiated by binding to a transmembrane receptor, followed by a series of phosphorylations. It is likely that glucocorticoid-induced insulin resistance results from an alteration at one or more of the levels of the signaling cascade. In the chicken, corticosterone can cause insulin resistance along with impaired muscle growth and, in the long term, excessive fattening. Dupont et al. (1999) showed that corticosterone impaired insulin signaling in the liver and also, to some extent, in the muscle of chickens, and that it contributed to impairment in growth.
Leptin is derived from both liver and adipose tissue in chickens. In most mammal species, the major source is the adipose tissue. It acts as a metabolic signal between peripheral lipid stores and the central nervous system and plays an important role in the regulation of food intake, energy expenditure, and reproduction (Friedman and Halaas, 1998; Clarke and Henry, 1999). As adiposity increases, so does leptin secretion, which signals the hypothalamus to suppress feed intake and increase energy expenditure (Zhang et al., 1994). The data reported here showed that leptin levels were consistently higher in ED birds than in SKIP birds. The pattern of leptin secretion, however, was remarkably similar in both sets of birds. Some studies (Paczoska-Eliasiewicz et al., 2003) have indicated that in chickens, leptin might be involved in the adaptation to starvation because of its role in the attenuation of follicular apoptosis normally associated with fasting. Plasma leptin levels reflect the energy status of an individual. The elevated leptin levels in ED birds may be a reflection of the less dramatic fluctuations in feed supply to these birds. Several authors (Caprio et al., 2001; Cassy et al., 2004) have indicated a role for leptin in the reproductive function of broiler breeders. According to Caprio et al. (2001), at low concentrations leptin acts mainly at the central level. At higher concentrations, the central leptin receptors are protected by the saturable transport system of the blood-brain barrier. The peripheral receptors, however, are exposed to high leptin concentrations that exert an inhibitory action on gonadal steroidogenesis and ovulation. Cassy et al. (2004) suggested that leptin plays an important role in the dysfunction of the follicular hierarchy observed in standard broiler breeder hens fed ad libitum. Their study demonstrated the involvement of leptin in the nutritional control of reproduction in birds.
Increases in plasma triglycerides after feeding and subsequent decreases during the fasting period were observed in both ED- and SKIP-fed birds. The magnitude of the changes did not differ between ED and SKIP birds but the timing did. The point at which the crop emptied also marked the time at which plasma triglyceride levels began to decline. These changes were accompanied by increases in NEFA levels. The switch from an anabolic to a catabolic state was clearly defined. Uric acid is the primary route of waste nitrogen disposal in avian species. Increases in plasma uric acid concentration of ED and SKIP birds were noted between 8 and 12, and 20 and 24 h, respectively. These alterations in plasma uric acid may be indicative of changes in gluconeogenesis from amino acids. Most of the gluconeogenesis from amino acids takes place in the kidneys in chickens rather than in the liver (Watford et al., 1981).
In summary, our data showed that fasting resulted in a variety of changes in the plasma hormone and metabolite profiles of broiler breeders. These changes included increased T4, corticosterone, and glucagon. Plasma NEFA levels increased during fasting as a result of lipid mobilization to provide energy. This process of lipid mobilization was strongly stimulated by glucagon during fasting. Plasma insulin, T3, IGF-I, and triglyceride levels were reduced compared with fed birds, whereas plasma IGF-II levels were less responsive to feed deprivation. The process of refeeding reversed these effects by means of reciprocal changes in endocrine functioning (Buyse et al., 2002). Refeeding was accompanied by a significant increase in thermogenesis (Bennett et al., 1990). In general, the magnitude of these responses to fasting and refeeding was increased in SKIP compared with ED pullets. It is clear from our results that in spite of equal total feed intakes, feeding regimens were able to influence metabolism. After the onset of lay, most broiler breeders are fed every day. Whether the differences between ED and SKIP feeding during the rearing period continue to affect birds after sexual maturity is unclear. A comparison of previously SKIP- and ED-fed birds during the production period would help to define the ultimate consequences of these feeding regimens.
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ACKNOWLEDGMENTS |
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Received for publication May 16, 2007. Accepted for publication October 12, 2007.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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