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METABOLISM AND NUTRITION |
* Department of Biosystems, Katholieke Universiteit Leuven, 3001 Leuven, Belgium; Institut National de La Recherche Agronomique, UR83 Recherches Avicoles, F-37380 Nouzilly, France; Institut National de La Recherche Agronomique, UMR1236 Genetique et Diversite Animales, F-78350 Jouy en Josas, France; Gastroenterology Section, Department of Pathophysiology, Katholieke Universiteit Leuven, 3000 Leuven, Belgium; and || Division Nutrition, Department of Public Health, Katholieke Universiteit Leuven, 3000 Leuven, Belgium
1 Corresponding author: johan.buyse{at}biw.kuleuven.be
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Key Words: genotype • diet-induced thermogenesis • feed intake regulation • residual feed intake
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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To study macronutrient oxidation, stable isotope breath tests offer a safe and noninvasive method. A substrate labeled with 13C is ingested, followed by serial measurements of the 13C:12C ratio in the exhaled CO2 (Amarri et al., 1998). The recent development of a methodology to perform stable isotope breath test measurements in combination with indirect calorimetry with chickens has made the opportunity available to conduct research on nutrient oxidation in avian species (Buyse et al., 2004).
From 1976, starting from a base Rhode Island Red egg-laying line, 2 lines have been divergently selected for high (R+) or low (R–) residual feed intake. The selection criterion was defined as the difference between the observed feed intake and the feed intake predicted by regression between the feed intake and BW, BW gain, and egg mass production (Bordas and Mérat, 1984; Bordas et al., 1992). In addition to the direct selection response, several correlated responses were also observed. In spite of a higher feed intake, the R+ chickens were leaner than the R– birds (Tixier et al., 1988; El-Kazzi et al., 1995). The divergence in energy intake was associated with an increased activity in the R+ compared with the R– cockerels (Gabarrou et al., 2000) as well as an enhanced heat production in the R+ compared with the R– chickens in the males as well as the females, which was mainly due to higher diet-induced thermogenesis (Geraert et al., 1991; Gabarrou et al., 1997b, 1998).
The aim of the present study was to investigate the regulation of feed intake in R+ and R– cockerels, which are known to differ in DIT. The correlation between DIT and feed intake was assessed and the postprandial oxidation of U-13C6-glucose and decarboxylation of 1-13C1-Leu were analyzed with breath tests. Furthermore, endocrine functioning and key metabolites of the intermediary metabolism were examined and related to the feed intake-associated parameters.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Feed and drinking water were supplied for ad libitum consumption and feed intake of 10 animals per line was measured for 10 consecutive days.
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Heat Production Measurements
A detailed description of the respiratory unit is provided by Buyse et al. (1998). Briefly, it consisted of 3 light-and temperature-controlled climatic chambers, each containing 2 respiratory cells, a gas analyzer unit, and a data acquisition system. The respiratory cells (550 x 300 x 500 mm) were made of stainless steel with little insulation, and the inside temperature was measured by a resistance temperature detector (Pt-100, accuracy of 0.2°C, Farnell In One, Grace-Hollogne, Belgium). The paramagnetic O2 analyzer (ADC 02-823A, The Analytical Development Company, Hoddesdon, Herts, UK) and the infrared CO2 analyzer (ADC D/8U/54/A, The Analytical Development Company) were calibrated before every measurement by using gas mixtures with known (±0.001%) levels of O2 and CO2.
After the adaptation period in the respiratory cells, O2 and CO2 exchanges were measured continuously during the feed-deprivation period as well as during the subsequent refeeding period. The production of CO2 and the consumption of O2 of the cockerels were calculated from the differences between the gas concentrations of the fresh outside air (measured for 120 s every 20 min) and the outlet air of each cell. Heat production was calculated from these data according to the formula of Romijn and Lokhorst (1961):
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The term for urinary N excretion was omitted because it typically induces an error of 
1% (Romijn and Lokhorst, 1961). To assess DIT, the difference was calculated between the average value for heat production during the last 8 h of the feed-deprivation period before the lights were turned on (dark period: from 2200 h until 0600 h), on the one hand, and the heat production at every measuring point during the 7-h refeeding period (lighting period: from 0800 h until 1500 h), on the other hand. The DIT was then calculated as the area between the heat production-curves during feed deprivation and refeeding, and was expressed per gram of feed intake during that interval.
Stable Isotope Measurements
During the first half of each week of the experimental period, the postprandial carbohydrate oxidation was measured by using U-13C6-glucose (99% atom 13C, Bat 547 91191, Euriso-Top, Gif-Sur-Yvette, France) as described in detail in Buyse et al. (2004). After the 24-h feed-deprivation period, the control sample was collected: a 10-mL air sample was taken at the outlet side of each respiratory cell to determine the background 13CO2 that is normally produced by the chicken. Each air sample was taken with a 10-mL syringe and was delivered into a 10-mL Vacutainer tube (Labco Limited, Buckinghamshire, UK). Subsequently, the animals were weighed and given a single oral dose of 2 mg/kg of BW of U-13C6-glucose, which was dissolved in water in a concentration of 2 mg/mL. During the 7-h refeeding period, air samples were taken every 30 min to measure glucose oxidation.
During the second half of each week, the postprandial Leu decarboxylation rate was measured by using 1-13C1-Leu (99% atom 13C, Bat 547 91191, Euriso-Top), as described in detail by Swennen et al. (2007b). After the control sample was taken, the cockerels were weighed and intubated with 40 mg/kg of BW of 1-13C1-Leu, which was dissolved in water in a concentration of 20 mg/mL. During the first 4 h of the 7-h refeeding period, air samples were taken every 15 min to measure postprandial Leu decarboxylation. For both isotopes, the enrichment of 13 CO2 was measured by isotope ratio mass spectrometry, as described by Buyse et al. (2004).
Curve Fitting
The cumulative percentage dose recovery curves obtained for both isotopes showed a typical sigmoid pattern. Therefore, the data were fitted according to the Gompertz equation (Winsor, 1932):
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where Ot is the oxidation of U-13C6-glucose or the decarboxylation of 1-13C1-Leu at time t (min; % dose); A is the asymptote of the curve (% dose); and B and C are constants (min–1), and are indicative of the rate of increase and decrease in oxidation or decarboxylation during the ascending and descending phase of the curve, respectively. The point of inflection (POI) is calculated as B/C and is the time (min) at which the oxidation or decarboxylation rate is maximal. Finally, this maximal oxidation or decarboxylation rate (M; % dose x min–1) at POI is calculated as (A x C)/e.
Measurements and Sampling
The individual BW of the cockerels was recorded at the start of the experimental period under ad libitum-fed conditions, after feed deprivation, and after DIT measurements. During DIT measurements, feed intake was recorded for each animal. Blood samples were collected from a wing vein with a heparinized needle and syringe after feed deprivation and DIT measurements, and were immediately placed in crushed ice. At the end of the experiment, 10 ad libitum-fed cockerels per genotype were euthanized by cervical dislocation, and the liver and abdominal fat pad were removed and weighed.
DXA Measurements
At the end of the experiment, 6 chickens per genotype were killed by cervical dislocation and their body composition was determined by dual-energy x-ray absorptiometry (DXA) with a pencil beam total-body DXA scanner (Lunar DPX-L, Lunar Corp., Madison, WI). A detailed description of this methodology is provided by Swennen et al. (2004b). In short, the chickens were placed on the scanner on their backs and a scan of the whole body was made and analyzed by using Small Animal Total Body Scan research software (version 7.4a; Lunar DPX-L, Lunar Corp.). The detailed slow-scan mode was used, and a 4-mm-thick polystyrene plate was used as attenuating material. Dual-energy x-ray absorptiometry measurements estimate values for fat and lean tissue mass (g), fat percentage (%), bone mineral content (g), and bone mineral density (g/cm2). Body composition was then estimated by using these values and the linear equations previously established by Swennen et al. (2004b).
Plasma Metabolites and Hormones
Plasma glucose (IL Test kit, No. 182508-00, Instrumentation Laboratories, Zaventem, Belgium), triglyceride (IL Test kit, No. 181610-60), and uric acid (IL Test kit, No. 181685-00) concentrations were measured spectrophoto-metrically with an automated apparatus (Monarch Chemistry System, Instrumentation Laboratories). Plasma free fatty acid concentrations were measured with the Wako NEFA C test kit (Wako Chemicals GmbH, Neuss, Ger-many), an enzymatic colorimetric test modified for use in the Monarch Chemistry System. Plasma 3,5,3'-triiodothyronine (T3) and thyroxine (T4) concentrations were measured with a specific RIA as described by Darras et al. (1992). Plasma leptin levels were measured with a multispecies leptin RIA kit (Linco Research, Inc., St. Charles, MO) validated for chicken plasma (Dridi et al., 2000). All samples were run in the same assay to avoid interassay variability.
Statistical Analyses
All results were analyzed by ANOVA with genotype as the classification variable (SAS for Windows, Version 8e, 1998, SAS Institute Inc., Cary, NC). A P-value of <0.05 was considered the signification threshold. The nonlinear procedure was used to fit the Gompertz equation (Winsor, 1932) to the cumulative percentage dose recovery data of each chicken separately and to estimate the values for the parameters A, B, and C. The effect of nutritional state (after 24 h of feed deprivation or after 7 h of refeeding) on plasma hormone and metabolite levels was assessed, and genotype effects were analyzed for each nutritional state separately for these parameters.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Daily feed intake was 50% (P < 0.0001) higher in R+ compared with R– cockerels (Figure 1B).
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). During the subsequent 7-h refeeding period, this effect of genotype on heat production (per 7 h) was sustained and was even more pronounced (P < 0.0001; Figure 2B), resulting in a 44% difference between the 2 genotypes.
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). Because feed intake during the 7-h refeeding period was also 73% higher (P < 0.0001) in the R+ animals (Figure 2D), the DIT per gram of feed intake was not different between the genotypes (Figure 2E). The respiratory quotients (RQ) were not affected by genotype during the 24-h feed-deprivation period and approached fasting levels (0.7; data not shown). During the 7-h refeeding period, the RQ of the R+ cockerels was significantly (P < 0.05) higher compared with those of the R– chickens (R+: 0.909 ± 0.005; R–: 0.883 ± 0.008).
Stable Isotope Studies
The estimated parameters A, B, and C of the Gompertz curve and the calculated parameters POI and M are represented in Table 2. For the U-13C6-glucose oxidation measurements, the values for the asymptote (A) and the maximal oxidation rate at the POI (M) were significantly (P < 0.05) higher for the R+ than for the R– cockerels. The value of parameter B (rate of increase in oxidation), on the other hand, was higher in the R– chickens (P = 0.053). No effect of genotype was found on the values of the parameters C and POI.
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Organ Weights and Body Composition
The effect of genotype on organ weights and on body composition as assessed by DXA are presented in Table 3. The cockerels of the R– strain had a significantly (P < 0.0001) higher abdominal fat pad weight compared with the R+ chickens. In most R+ cockerels, no dissectible amount of abdominal fat was found, which explains the high error of means. The liver weight was significantly higher (P < 0.0001) in the R+ than in the R– animals.
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Plasma Metabolites and Hormones
Compared with the R+ cockerels, R– chickens were characterized by significantly (P < 0.05) higher plasma triglyceride levels in the feed-deprived state (Figure 3A). After refeeding, this effect of genotype on circulating triglyceride levels disappeared. Circulating levels of free fatty acids and glucose were not influenced by genotype, irrespective of nutritional state (Figure 3B and 3C, respectively). Genotype had an effect on plasma uric acid levels, with significantly augmented plasma concentrations of the R+ compared with the R– cockerels, and this for each nutritional state (P < 0.05 after feed deprivation and P < 0.001 after refeeding, respectively; Figure 3D). Refeeding after the 24-h feed-deprivation period resulted in significant (P < 0.0001) increases of the circulating levels of triglycerides, glucose, and uric acid, whereas the plasma levels of free fatty acids decreased significantly (P < 0.0001).
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). After refeeding, no effect of genotype was observed. Plasma T4 levels were not affected by genotype, independent of nutritional state (Figure 4B). Irrespective of nutritional state, R+ chickens were characterized by higher plasma leptin levels compared with those of R– cockerels (P < 0.01 after feed deprivation and P < 0.0001 after refeeding, respectively; Figure 4C). Refeeding after the 24-h feed-deprivation period caused a significant (P < 0.0001) increase in the plasma levels of T3 and a decrease in the plasma levels of T4, respectively, whereas no effect of nutritional state was observed on circulating leptin concentrations.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Already after 7 generations of selection, Bordas and Mérat (1984) observed a significant (17.6%) difference in feed intake between cockerels of the R+ and R– lines. This divergence between the strains increased throughout the course of selection, resulting in a difference of 49% in the 17th generation (Gabarrou et al., 1998). The 50% higher ad libitum feed intake by the R+ cockerels compared with the R– cockerels found in the present experiment corroborates these findings.
Heat Production and DIT
It has been reported previously that the digestive capacity is similar in both lines (Geraert et al., 1991; Gabarrou et al., 1997b); thus, the higher feed intake by the R+ cockerels resulted in a higher ME intake, which could be compensated for by an enhanced energy expenditure or by changes in body composition (Geraert et al., 1991) or both. Indeed, heat production during the refeeding period was significantly higher in the R+ cockerels compared with the R– cockerels, as observed previously (Geraert et al., 1991; Gabarrou, 1996; Gabarrou et al., 1997b). Although not monitored in this study, a difference in the physical activity of the chickens might partly explain the divergence in heat production between the 2 strains. The effective caloric value of a diet has been shown to be dependent on behavioral patterns (Skinner-Noble et al., 2005), and bird activity has been known to have an impact on heat production. Indeed, it has been proven that the chickens of the R– line are less active and spend more time resting compared with the R+ chickens (Braastad and Katle, 1989; Gabarrou et al., 2000). However, the activity-induced heat production accounted for only 25 to 36% of the divergence between lines (Gabarrou et al., 1997b). Consequently, the largest proportion of the difference in heat production between the 2 strains can be explained by a difference in DIT (Gabarrou, 1996). The difference in DIT between the R+ and R– cockerels was 90% in the present study, which is larger than the difference of 75% reported by Gabarrou et al. (1998). However, in the latter study, the DIT was calculated by subtracting the average heat production during fasting from the average heat production during refeeding. In our experiment, the DIT was determined as the area between the heat-production curves during the last 8 h of feed deprivation (in the dark) and the 7-h refeeding period, taking every measuring point into consideration. Because this is a more accurate method of calculation, it is possible that the DIT has been underestimated in previous research. Finally, the body composition of the cockerels might play a role in the increased heat production and DIT observed in the R+ chickens compared with the R– chickens. Indeed, the contribution of fat free mass to metabolic rate is much larger than that of fat mass (Lührmann et al., 2001). In the present experiment, the R+ chickens had a significantly (P < 0.05) increased lean tissue mass compared with the R– chickens, as is discussed later, which could have an effect on heat production. However, because the body composition of the chickens used in the metabolic studies was not determined, it is difficult to draw a solid conclusion regarding the effect of body composition on heat production in the present study.
Gabarrou et al. (1998) stated that the divergence in feed intake between the lines was maximal at the onset of light. Our present study corroborates these findings because the difference in feed intake between the 2 genotypes was most pronounced (73%) during the 7-h refeeding period following 24 h of feed deprivation, compared with the 50% difference under ad libitum conditions. This more pronounced difference in feed intake at the onset of light contributed to the increased divergence in heat production and DIT measured during the same refeeding period. When DIT was corrected for the amount of feed consumed, no difference between lines could be observed, indicating that DIT had no feedback effect on feed intake. The hierarchic oxidation model of Stubbs et al. (1997), which was propagated based on research with adult mammals, links DIT to feed intake: a higher DIT has a stronger negative feedback effect on subsequent feed intake. In previous studies, an effect of neither genotype (genetically fat and lean lines, age-matched broiler vs. layer chickens) nor diet composition (isoenergetic substitutions between protein and fat) was found on DIT (Swennen et al., 2004a, 2006, 2007a). When these data were combined with our present results, the role of DIT in the regulation of feed intake did not seem to be very important, or might not even exist in poultry, in contrast to mammals.
Stable Isotope Measurements
According to the model of Stubbs et al. (1997), proteins are preferentially combusted, followed by carbohydrates and finally fat. Also for humans, the protein content of a diet is one of the major determinants of DIT and plays a key role in BW regulation through satiety-related DIT (see review by Westerterp, 2004). Therefore, according to this model, and considering the large difference in DIT between the genotypes, the R+ cockerels would be expected to have an elevated oxidative decarboxylation of Leu. However, although the decarboxylation of 1-13C1-Leu was somewhat higher in the R+ compared with the R– chickens, this difference was not statistically significant (P > 0.05). 1-13C1-Leucine was used as a tracer because it allows the study of the oxidative decarboxylation of 
-ketoisocaproate, which is the first irreversible step of Leu degradation (Wolfe, 1992). The resulting isovaleryl coenzyme A can then be used for the synthesis of other compounds, such as glucose, amino acids, or fatty acids (Berg et al., 2002). Although there was no genotype effect on oxidative decarboxylation, it is possible that the metabolic fate of isovaleryl coenzyme A was not the same for both strains. The chickens of the R– line will probably use it as a substrate for lipid synthesis, as reflected in the higher abdominal fat pad weight and increased fat tissue mass.
The R+ chickens oxidized a higher proportion of the administered dose of U-13C6-glucose than did the R– cockerels (A parameter), which was reflected in a higher maximal oxidation rate (M parameter) in the former group. Next to the higher feed intake, and consequently, the higher carbohydrate uptake, of the R+ compared with the R– chickens, it can be inferred that the R+ cockerels used relatively more of the ingested glucose as an energy source, which is in agreement with the higher RQ value of these chickens. In contrast, the R– chickens probably used glucose as a precursor for lipid synthesis.
It is possible that the decarboxylation of 1-13C1-Leu and the oxidation of U-13C6-glucose were underestimated in the current experiment because of a "dilution" effect. The R+ cockerels had a significantly higher feed intake than the R– chickens, and consequently, dietary Leu and glucose intake were also elevated in the former group. The doses of the isotopes administered were based on the (comparable) BW of the animals, and were thus similar for both groups. Therefore, the isotopes administered to the R+ chickens were "diluted," because they were mixed with a larger amount of unlabeled substrate from the diet. Consequently, a significant effect of genotype on 1-13C1-Leu decarboxylation was probably masked and the difference in U-13C6-glucose between the 2 genotypes might have been underestimated.
Body Composition
The abdominal fat pad weight was significantly decreased in the R+ chickens compared with the abdominal fat content of the R– chickens, the latter having a normal fat content for adult cockerels. This effect of genotype on fatness was already observed in the 7th and 10th generation of selection (Bordas and Mérat, 1984; Tixier et al., 1988) and has occurred progressively throughout the course of selection (El-Kazzi et al., 1995; Lagarrigue et al., 2000). The R– chickens had an elevated fat tissue mass as estimated by DXA, which supports the above-mentioned statement that the R– chickens preferentially used the ingested nutrients as a substrate for lipogenesis. On the other hand, the significantly elevated liver weight of the R+ cockerels seems to contradict these findings, considering that the liver is the major site of lipogenesis in birds (Leveille et al., 1975). Although a proportional increase in liver weight has been observed previously in the R+ chickens (Tixier et al., 1988; Lagarrigue et al., 2000), a plausible explanation is lacking. Because the liver is an organ with a high metabolic activity, Gabarrou et al. (1997b) suggested that its enlargement might contribute to a higher heat production in the R+ cockerels. These authors showed that hepatic mitochondria from R+ cockerels had a higher stimulated respiration rate and oxidative capacity than those from R– cockerels (Gabarrou, 1996).
The R+ animals had a higher lean tissue and protein mass. These findings are in agreement with those of El-Kazzi et al. (1995), who reported that the lipid content of skin and breast muscle was increased in R– chickens of the 17th generation. Furthermore, the ash weight, estimated from the bone mineral content measured with DXA, was (nearly significantly) higher in the R+ compared with the R– chickens. This is probably due to the heavier legs and wings in the R+ line, which is a known correlated selection response (Zein-el-Dein et al., 1985; Bordas et al., 1992, 1996; El-Kazzi et al., 1995; Bordas and Minvielle, 1999).
Plasma Metabolites and Hormones
The effects of feed deprivation and subsequent refeeding on circulating levels of metabolites and hormones are in agreement with previous reports (Buyse et al., 2002; Swennen et al., 2005, 2006). A more detailed discussion is provided by those authors.
There were no effects of genotype on the plasma free fatty acid and glucose concentrations, corroborating the findings of Gabarrou et al. (1998). The lack of a genotype effect on plasma glucose seems to contradict the elevated U-13C6-glucose oxidation levels in the R+ chickens compared with the R– chickens, but this is probably due to the strict carbohydrate homeostasis in avian species (Simon, 1991).
The lower plasma triglyceride levels in the R+ chickens during feed deprivation might be due to an elevated uptake of triglycerides by peripheral tissues, where they will be used as an energy source. This would contribute to the higher heat production during feed deprivation in these animals. After refeeding, dietary energy sources become available and no effect of genotype on circulating triglyceride levels was observed, which is in agreement with the findings of Gabarrou et al. (1998). Circulating uric acid levels were higher in the R+ cockerels, independent of nutritional state, as previously observed by Gabarrou et al. (1996). Because plasma uric acid is a reliable biomarker for amino acid degradation in birds (Goldstein and Skadhauge, 2000), this indicates an elevated amino acid oxidation in the R+ compared with the R– chickens. These results support the tendency toward higher 1-13C1-Leu decarboxylation by the former animals.
During feed deprivation, the R+ chickens had lower T3 plasma concentrations than the R– cockerels, whereas after refeeding, no difference was found between genotypes. Because the level of T3 in the plasma is, in most cases, positively correlated with heat production (Klandorf et al., 1981), this seems to contradict the higher heat production in the R+ group. Gabarrou et al. (1997a, b) also observed a lower plasma T3 concentration in the R+ chickens during fasting in combination with an increased maximum T3-binding capacity of hepatic nuclei. This indicates a higher concentration of T3-receptors compared with the R– chickens, which could be related to the divergent feed intake levels of these genotypes (Gabarrou et al., 1997a). The greater concentration of T3-receptors in the R+ cockerels may favor the capacity of the thyroid hormones to stimulate heat production. Otherwise stated, the increased T3-binding capacity might explain the higher heat production in the R+ chickens observed in the present experiment, in spite of lower or similar plasma T3 levels after feed deprivation and refeeding, respectively. In addition, the higher T3-binding in the liver, in combination with the increased liver weight of the R+ cockerels, may point to a different compartmentalization of T3, preferentially in the liver and less in the plasma compartment for the R+ animals. Plasma T4 levels were not affected by genotype, independent of the nutritional state, confirming previous reports (Gabarrou et al., 1996, 1997a,Gabarrou et al., b).
In mammals, leptin has been described as a satiety hormone that is secreted mainly by adipose tissue. In poultry, leptin synthesis occurs in the liver as well as in adipose tissue (Ashwell et al., 1999; Taouis et al., 2001). Because the R+ chickens had practically no abdominal fat, in contrast to the R– chickens, the elevated plasma leptin levels in the R+ cockerels suggest that the liver might be the major site of leptin production. This hepatic expression of leptin in chickens is thought to be associated with the role of this organ in lipogenesis (Taouis et al., 1998). The lower body fat content of the R+ chickens seems to contradict this. A single leptin injection (Cassy et al., 2004) as well as constant leptin infusion (Dridi et al., 2005) induces a significant reduction in feed intake in chickens, indicating that the satiating effect of leptin described in mammals also occurs in the chicken. However, in the present study, circulating leptin concentrations were significantly increased in the R+ chickens, as was their appetite. The satiating effect of leptin seems to be overruled by other factors that stimulate feed intake, which might be related to the selection procedure. Indeed, Cassy et al. (2004) provided evidence that layer and broiler chickens differ in their responsiveness to leptin, suggesting a genotype effect. Finally, it is possible that a correlation exists between the high leptin levels in plasma and the increased heat production of the R+ chickens. Research with humans (Salbe et al., 1997) and with rodents (ob/ob mice, Halaas et al., 1995; Hwa et al., 1997) has shown that energy expenditure is positively correlated with plasma leptin concentrations. Thus, the role of leptin in these strains of chickens selected for residual feed intake should be investigated further.
In conclusion, in spite of clear differences in DIT between the R+ and R– chickens, we observed no feedback effect of DIT on feed intake. In addition, we observed no significant genotype effect on 1-13C1-Leu decarboxylation, although this difference might have been underestimated because of the difference in feed intake. Thus, based on the present experiment, the model of Stubbs et al. (1997) could not be corroborated for these strains of chickens. Together with the results of previous studies (Swennen et al., 2004a, 2006, 2007a), this suggests that DIT plays little or no role in the regulation of feed intake in chickens. The significant difference in U-13C6-glucose oxidation combined with the pronounced differences in body composition indicate that the R+ cockerels used the ingested glucose primarily as an energy source, whereas the R–chickens used it for lipid synthesis. This difference in nutrient utilization was reflected in the plasma uric acid levels, the RQ values, and the divergent heat production by both genotypes.
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ACKNOWLEDGMENTS |
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Received for publication January 24, 2007. Accepted for publication May 11, 2007.
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