Model 1: The overall efficiency of digestible energy utilisation for fat and protein deposition The efficiency of digestible energy utilisation for fat and protein was 0.75 and 0.28
respectively. This result was based on the multiple linear regressions using the data from all treatment groups (Table 11, Model 1).
Table 5.11. Regression equations to predict the efficiency of digestible energy utilisation for protein (kp) and fat (kf) deposition
diet Model regression equation kf kp R2
Basal, NEAA1, NEAA2 1 iDEI= -3.56 +3.9 ERP+1.33ERF 0.75 0.28 0.56 (9.24) (0.97) (0.51)
Basal, NEAA1, NEAA2 2 iDEI= 28.3 +1.62 ERF 0.62 - 0.22
(6.19) (0.66)
Basal, NEAA1, NEAA2 3 iDEIpfd= 16.0 + 1.51 ERF 0.66 - 0.25 (5.28) (0.56)
Numbers in the parentheses are the standard errors of above coefficient.
Model 1 multiple linear regression cross all treatment groups, iDEI= intercept + (1/kf) ERF+ (1/kp) ERP. Model 2 linear regression iDEI= intercept + (1/kf) ERF, data from Basal, NEAA1 and NEAA2 was fitted, assumed extra energy intake would not affect protein retention and the intercept presented the protein deposition and maintenance energy requirement.
Model 3 linear regression iDEIpdf= intercept + (1/kf) ERF, iDEIpdf is the net energy after subtracting the energy requirement for protein retention.
Model 2: The efficiency of NEAA utilisation for fat deposition
The kfN value was estimated as 0.62 using linear regression model with the data from basal,
NEAA1 and NEAA2 treatment groups (see Table 11, Model 2). This estimation is based on the assumption that the extra digestible energy from NEAA intake would not increase the protein deposition but increase the fat deposition.
Model 3: Corrected to protein deposition free ileal digestible energy
The results showed that both the protein and fat deposition systematically increased when the birds consumed more NEAA. Further analysis was taken to predict the efficiency of digestible energy utilisation for fat deposition from extra NEAA intake. The efficiency of digestible energy utilisation for fat deposition from extra iDEIfpd was 0.66; this result was based on the linear regression using the data from Basal, NEAA1 and NEAA2 treatment groups (Table 11, Model 3). The iDEIfpd was provided not only from extra NEAA intake,
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but also from digestible starch intake (see Table 5.7). Thus, the efficiency of NEAA utilisation for fat deposition calculated using this formula:
Rewriting the equation
Where:
X is a fraction of additional digestible energy from NEAA intake toward fat deposition. Y is a fraction of additional digestible energy from starch intake toward fat deposition. kfs is the efficiency of digestible energy utilisation for fat deposition from starch (used
value 0.75 from De Groote, 1974).
kfNis the efficiency of digestible energy utilisation for fat deposition from NEAA.
This assumes that the maintenance energy requirements coming from digestible starch and NEAA were of similar proportion. From this calculation it is clear that the kfN would be
0.63.
5.4.9. The theoretical efficiency to produce carbon skeleton from amino acids
The energetic efficiency for essential amino acids to produce carbon skeleton ranged from 0.66 to 0.93 with an average of 0.85. For non-essential amino acids the energetic efficiency to produce carbon skeleton ranged from 0.72 to 0.89 with an average of 0.80 (Table 5.12).
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Table 5.12. Energetic efficiency of amino acids to produce carbon skeleton, based on the energy balanced description
AA Formula MW(g/mol)1 Nitrogen (g/mol) GE (kJ/g AA)2 N% (g/g AA)3 g uric acid4 kJ/uric acid5 Efficiency6
NEAA
Glycine C2H5NO2 75.0 14 17 0.186 0.559 4.70 0.72
Serine C3H7NO3 105 14 16.6 0.133 0.399 3.36 0.80
Glutamine C5H10N2O3 146 28 20.1 0.190 0.571 4.83 0.76
Alanine C3H7NO2 89.0 14 22.8 0.157 0.471 3.96 0.83
Aspartic acid C4H7NO4 133 14 14 0.105 0.316 2.65 0.81
Proline C5H9NO2 115 14 28.1 0.122 0.365 3.06 0.89
Average of NEAA 0.80
Essential amino acids (EAA)
Arginine C6H14N4O2 174 56 23.9 0.322 0.966 8.11 0.66 Cysteine C3H7NO2S 121 14 21.6 0.116 0.347 2.92 0.86 Histidine C6H9N3O2 155 42 24.6 0.271 0.813 6.83 0.72 Isoleucine C6H13NO2 131 14 31.6 0.107 0.321 2.69 0.91 Methionine C5H11NO2S 149 14 21.2 0.094 0.282 2.37 0.88 Phenylalanine C9H11NO2 165 14 31.6 0.085 0.255 2.14 0.93 Threonine C4H9NO3 119 14 20.3 0.118 0.353 2.97 0.85 Tyrosine C9H11NO3 181 14 27.2 0.077 0.232 1.95 0.93 Valine C5H11NO2 117 14 29.5 0.120 0.359 3.02 0.90 Tryptophan C11H12N2O2 204 28 30.2 0.137 0.412 3.46 0.88 Average of EAA 0.85 Overall average 0.83 1
MW(g/mol) is the molecular weight (g/mol AA). 2GE; is the GE per gram AA (adapted from Van Milgen 2002). 3 N% is the nitrogen percentages calculated as molecular weight of nitrogen content in AA divided by the molecular weight of the AA. 4g uric acid produced from AA calculated as N content multiplied by 3. 5kJ/uric acid the energy required to produce the uric acids calculated as gram uric acid multiplied by 8.37 kJ. 6Efficiency of the energy retained in carbon chain pivot.
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5.5. Discussion
The experiment was designed to assure that the intake of the basal diet was identical among the treatment groups. Therefore, it was anticipated that the excess supply of NEAA would have an effect on fat deposition. Indeed, the additional energy from NEAA resulted in increase in both the fat and protein deposition. This finding suggests that the levels of extra NEAA intake was either insufficient or was not completely utilised for fat growth. Also, the birds fed the diet with additional NEAA had higher essential and NEAA intake compared with those fed basal diet.
5.5.1. Feed intake and performance
The growth performance parameters for live body weight, daily gain and feed per gain showed the superiority of the birds fed extra energy in form of NEAA compared to those fed the basal diet. It is known that bird performance improves with the increase in energy intake (Shyam et al., 2007; Boekholt et al., 1994; Leeson, 1996 b; Arafa et al., 1983). Broiler body weight gain and the feed per gain improved when the birds were fed a diet supplemented with 2% NEAA between 5- 21 day of age (Corzoa et al., (2005). Aletor et al., (2000) also reported the feed per gain improved when broiler diets were supplemented with NEAA. Moran, (2011) reported that the deficiency of NEAA (glycine-serine and proline) with low crude protein diet could reduce the growth performance.
5.5.2. Description of body components growth rates
In our experiment, the protein deposition was increased when the birds were fed the B+NEAA1 diet, but no further increases were observed when the birds consumed more NEAA with the B+NEAA2 diet. For fat deposition, the birds fed the B+NEAA1 diet had similar fat deposition to the basal diet, but the fat deposition increased when the birds consumed more NEAA with the B+NEAA2 diet. Extra NEAA intake appeared to be supporting protein deposition and once the requirement for protein deposition was met, the excess of NEAA was used for fat synthesis. This finding suggests that a deficient supply NEAA could cause a breakdown of EAA for formation of NEAA, which means a limitation of EAA for protein synthesis and then a reduction in protein deposition. Moran and Stillborn, (1996) showed that added glutamic acid to low crude protein diet improved live weight gain in broiler chickens. The fat deposition was increased when the birds were fed the B+NEAA2 diet compared to those fed basal diet,
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this is because of the additional AA were being converted into lipids by lipogenesis process, as a mechanism of store nutrients in the body. The broiler carcass fat content increases when the glycine and glutamic AA were added to low protein diet balanced with EAA (Deschepper and de-Groote, 1995).
It appears that the provision of NEAA in broiler diets is important to prevent AA deficiencies. The NEAA should be considered in broiler industry to improve the growth performance, particularly when boilers have restricted feed intake.