Dietary factors

metabolizable energy concentration. Dietary ME content is widely acknowledged to exert a dominant role in the regulation of food intake in growing poultry. Boomgaardt and Baker (1973) examined the effects of dietary ME concentration on the response of chicks to graded doses of SAA. Cursory evaluation of their results indicates three distinct growth response curves for the three ME concentrations used (Fig. 14.12). However, the

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Arginine intake (mg day-1)

Fig. 14.10. Daily weight gain responses of turkey poults (•) and young chicks (□) in relation to daily arginine intake. (From D'Mello and Emmans, 1975; source of data: turkeys, D'Mello and Emmans, 1975; chicks, D'Mello and Lewis, 1970. Reproduced with permission of British Poultry Science Ltd.)

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Methionine + cystine intake (mg day-"1)

Fig. 14.11. Weight gain responses of growing rats (□), slow-growing chicks (•), fast-growing chicks (o) and turkey poults (A) in relation to methionine and cystine intake. (From D'Mello, 1976; source of data: rats, Stockland eta!., 1973; slow-growing chicks, Boomgaardt and Baker, 1973; fast-growing chicks, D'Mello, 1973b; turkeys, D'Mello, 1976. Reproduced with permission of British Poultry Science Ltd.)

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Dietary methionine + cystine concentration (g kg-1)

Fig. 14.12. Daily growth rates of young chicks in relation to dietary methionine + cystine and metabolizable energy concentrations. Energy levels (MJ kg 1): (•) 10.9; (o) 12.6; (A) 14.2. (From D'Mello, 1979; source of data: Boomgaardt and Baker, 1973. Reproduced with permission from Butterworth-Heinemann Ltd.)

Dietary methionine + cystine concentration (g kg-1)

Fig. 14.12. Daily growth rates of young chicks in relation to dietary methionine + cystine and metabolizable energy concentrations. Energy levels (MJ kg 1): (•) 10.9; (o) 12.6; (A) 14.2. (From D'Mello, 1979; source of data: Boomgaardt and Baker, 1973. Reproduced with permission from Butterworth-Heinemann Ltd.)

efficiency of utilization of these amino acids is unaffected by energy content of the diet since a single response curve is obtained on plotting weight gain against methionine + cystine intake (Fig. 14.13). It is clear that dietary ME, within the range tested, exerts its effects principally through alterations in food intake and without affecting amino acid utilization.

amino acid imbalance. As discussed in Chapter 7, dietary amino acid imbalance precipitates its adverse effects by reducing food intake while the efficiency of amino acid utilization remains unimpaired (Harper and Rogers, 1965). However, the results of Morris et al. (1987) presented in Fig. 14.2 and those of Mendonca and Jensen (1989) and Abebe and Morris (1990b) appear to challenge this universally accepted rule. The responses in Fig. 14.2 indicate that as CP content increases from 140 to 280 g kg-1 diet there is a marked and progressive reduction in the efficiency of utilization of the first-limiting amino acid, lysine. Both the positive displacement of the response curves and the reduction in the slope of these curves, particularly at the higher CP concen-

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Methionine + cystine intake (mg day-1)

Fig. 14.13. Daily chick growth and methionine + cystine intake at three dietary concentrations of metabolizable energy (MJ kg 1): (•) 10.9; (o) 12.6; (A) 14.2. (From D'Mello, 1979; source of data: Boomgaardt and Baker, 1973. Reproduced with permission from Butterworth-Heinemann Ltd.)

trations (260 and 280 g kg-1 diet) imply substantial decreases in the efficiency of utilization of lysine. It will be noted that the displacement of the response curves occurs even at suboptimal levels of dietary CP. Abebe and Morris (1990b) attributed these responses to an effect of 'general imbalance caused by the excess of amino acids absorbed following digestion of a high protein diet'. Such an explanation is inconsistent with the evidence and with the hypothesis of Harper and Rogers (1965). This hypothesis was originally developed on the basis of metabolic studies with rats and has not been exhaustively tested in supplementation trials with pure amino acids. Accordingly, D'Mello (1990) conducted an investigation employing crystalline amino acids to bring about changes in CP concentrations and degree of imbalance in lysine-deficient diets fed to young chicks. Three basal diets composed mainly of maize gluten meal, wheat, glucose and amino acids were each formulated to contain 5.1 g lysine kg-1 dry matter (DM). The first, containing 225 g CP kg 1 DM served as the control diet. The second and third basal diets were similar to the control apart from the inclusion of a moderately or severely imbal-anced mixture of amino acids devoid of lysine. These mixtures were added at the expense of glucose thereby increasing CP concentrations to 315 g kg-1 DM. Each of the three basal diets was supplemented with graded levels of lysine. The relatively poor growth performance of chicks fed the control diet was depressed further by additions of the two amino acid mixtures lacking lysine (Fig. 14.14). This follows the classic pattern established with the rat (Harper and Rogers, 1965). The severity of the adverse effects was directly proportional to the degree of imbalance in the mixtures. In all three dietary regimes graded growth responses occurred to lysine supplementation but chicks in the two imbalanced series failed to attain growth rates comparable to those in the control regimes at equivalent levels of lysine addition. Consequently, growth remained depressed, relative to control, in the imbalanced groups at all levels of lysine addition, the retardation being particularly marked in the severely imbalanced groups. However, a highly significant linear relationship was observed between lysine intake and weight gain with all data points contributing to a single response curve. The appearance on a single response curve of all data points drawn from three diverse dietary regimes suggests that neither CP level nor severity of amino acid imbalance exerts any effect on lysine utilization. This finding is entirely consistent with the observations by Harper and Rogers (1965) and their hypothesis therefore remains intact. It thus appears unlikely that amino acid imbalance is a satisfactory explanation for the protein effect on lysine utilization (Fig. 14.2) and the issues raised by the data of Morris et al. (1987) and others (Mendonca and Jensen, 1989; Abebe and Morris, 1990a,b) remain essentially unresolved.

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100 200 300

Lysine intake (mg day-1)

Fig. 14.14. Daily weight gain and lysine intake of chicks fed diets containing 225 g crude protein kg 1 dry matter (•) or similar diets supplemented with a moderately (■) or severely (A) imbalanced mixture of amino acids lacking lysine which increased crude protein content to 315 g kg-1 dry matter. (Source of data: D'Mello, 1990.)

effects of vitamins and coccidiostats. A number of other nutritional factors affect the growth responses of poultry to amino acids by modulating food intake. Thus differences in responses to methionine + cystine induced by feeding chicks adequate or vitamin B12-deficient diets may be explained in terms of variations in food intake (D'Mello, 1979). Although Willis and Baker (1980) suggested the existence of a strik ing interaction between lasalocid (an ionophore coccidiostat) and SAA in diets severely limiting in these amino acids, inspection of Fig. 14.15 indicates that SAA utilization is unaffected by lasalocid supplementation. The coccidiostat merely enhances food intake in chicks fed the deficient diets resulting in higher intakes of SAA with consequent improvements in growth.

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100 200 300 400 500 600 700 800 900 1000 Methionine + cystine intake (mg 6 days-1)

Fig. 14.15. Weight gain and methionine + cystine intake of chicks fed purified diets without (•) or with (o) lasalocid, 125 mg kg-1. (From D'Mello, 1988; source of data: Willis and Baker, 1980. Reproduced with permission of The World's Poultry Science Association.)

100 200 300 400 500 600 700 800 900 1000 Methionine + cystine intake (mg 6 days-1)

Fig. 14.15. Weight gain and methionine + cystine intake of chicks fed purified diets without (•) or with (o) lasalocid, 125 mg kg-1. (From D'Mello, 1988; source of data: Willis and Baker, 1980. Reproduced with permission of The World's Poultry Science Association.)

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