Cyst(e)ine imbalance and its effect on methionine precursor utilization in chicks
2008
Dilger, R.N. | Baker, D.H.
Five 9- or 12-d chick growth bioassays were done in batteries using 2 Met-deficient diets: a purified AA-based diet containing (by analysis, as-fed) 20.3% CP, 0.12% Met, and 0.05% cyst(e)ine; and an AA-fortified corn-peanut meal diet containing (by analysis, as-fed) 19.0% CP, 0.22% Met, and 0.23% cyst(e) ine. Feed-grade DL-Met (DL-M; 99%) was compared with feed-grade DL-OH-Met, Ca (OH-M; 84%). When the purified diet was modified to contain 0.12% Met and 0.20% or greater cyst(e)ine, slope-ratio assays involving graded dosing of DL-M (0, 404, 808, and 1,212 mg of DL-M/kg) or isosulfurous levels of OH-M resulted in linear (P < 0.01) BW gain and G:F responses. Multiple linear regression analysis (BW gain vs. supplemental sulfur intake, R² = 0.98) resulted in a mean bioefficacy estimate of 78.1% for OH-M vs. DL-M (equivalent to 65.6% on a supplemental compound basis). In assay 3, the purified diet was modified to be equally deficient in Met and cyst(e)ine [i.e., 0.12% Met, 0.12% cyst(e)ine]. When this diet was supplemented with either 404 mg of DL-M/kg or 476 mg of OH-M/kg, BW gain and G:F responded (P < 0.01) markedly to either compound, and differences between DL-M and OH-M were not significant (P > 0.10). Assays 4 and 5 used the corn-peanut meal basal diet containing 0.22% total Met and 0.23% total cyst(e)ine. In both assays, addition of either 465 mg of DL-M/kg or 554 mg of OH-M/kg resulted in increased (P < 0.01) BW gain and G:F, regardless of dietary cyst(e)ine concentration. In the absence of excess cyst(e)ine, BW gain responses to DL-M and OH-M were similar, but when 0.10% excess cyst(e)ine was provided as L-cystine or feather meal, DL-M responses tended to exceed those of OH-M. Moreover, this small excess of dietary cyst(e)ine, regardless of source, depressed (P < 0.01) feed intake and BW gain when added to the basal diet. Overall, these results suggest that excess dietary cyst(e)ine, when included in Met-deficient diets, has the potential to be both anorexigenic and pernicious to OH-M utilization.
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