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Biomedical subjects

G M Pesti

Publications and source records attributed to G M Pesti.

96 records · Page 6Linked to original sources

Choline/methionine nutrition of starting broiler chicks. Three models for estimating the choline requirement with economic considerations.

Experiments were conducted to test the hypothesis that metabolically labile methyl groups and not methionine per se are limiting the growth of starting broiler chicks fed corn-soy-grease diets formulated to meet NRC (1977) recommendations (except for methionine). The basal diet contained approximately 23% protein, 3200 kcal ME/kg. 32% methionine, .42% cystine, and 1300 ppm choline. In the first two experiments the diets were fed to quadruplicate lots of 10 chicks in battery brooders. Average weight gain (g) and feed per unit gain for supplements of methyl group sources were: 1) methionine: 424, 1.48; 2) choline Cl: 406, 1.49; and 3) betaine HCl: 416, 1.48. These values were not significantly different from one another (P greater than .05) but were significantly different (P less than .05) from the values for the basal (362, 1.57) and from the DL-homocystine supplemented groups (376, 1.56). This indicated that methyl group utilization was not impaired by a lack of the carbon skeleton of methionine. Five 3-week assays with five groups of 10 chicks per treatment (1050 chicks) were conducted to determine the choline requirement using the basal diet without supplemental methionine. Results from the five assays were pooled in computing regressions. Significant regressions (P less than .05) were found for broken-line linear (R2 = .630), quadratic (R2 = .556), and saturation kinetic (R2 = .642) models. The requirement was determined to approximately 2130 ppm by the broken-line linear model. The most economic feeding levels were estimated to be 4100 and 1910 ppm by the quadratic and saturation kinetic models, respectively. The economic implications of the three models are discussed.

Animal Nutritional Physiological Phenomena↗

Sulfur amino acid and methyl donor status of corn-soy diets fed to starting broiler chicks and turkey poults.

Experiments were conducted to determine the effects of supplementing corn-soy-bean meal-white grease diets with sulfur amino acids and methyl group donors for starting broiler-strain chicks. The diets (23% protein and 3200 kcal ME/kg) were fed to quadruplicate lots of chicks in battery brooders. The diets were calculated to contain .37% methionine, .37% cystine, and 1499 mg/kg choline. Chemical and microbiological assays yielded values of .32% and .42% for methionine and cystine content respectively. Results of 5 chick experiments showed that supplementing this diet with .23% DL-methionine significantly (P less than .05) improved 3 week-gain (375 vs. 415 g) and feed/gain (1.54 vs. 1.47) over that obtained with the basal diet. When L-cystine and 2(CaSO4).H2O failed to give a significant (P greater than .05) response, compounds capable of donating methyl groups were fed. Significant (P less than .05) responses in gain (404 and 420) and feed/gain (1.48 and 1.51) over the basal were obtained with choline and betaine. These responses were not significantly (P greater than .05) different from that obtained with methionine. Serine and sodium formate failed to give consistent responses. Using a poult diet of 28% protein and 2800 kcal ME/kg, a significant (P less than .05) response to DL-methionine was again observed, with intermediate responses to betaine, choline, and serine. It is concluded that (within the limits of the experimental model) corn-soy type diets contain an adequate amount of total sulfur amino acid for chicks, but not poults, when sufficient choline or betaine are provided.

Amino Acids, Sulfur↗

Influence of ascorbic acid on selenium nutrition in the chick.

Experiments were conducted to determine the nature of the effect of dietary ascorbic acid on selenium nutrition in the chick. Results showed that ascorbic acid resulted in increased activities of the selenium-containing enzyme glutathione peroxidase in plasma, accompanied by an apparent reduction in the dietary selenium requirement of the vitamin E-deficient chick. The ascorbic acid contents of plasma, liver, kidney and adrenals were not affected by selenium or vitamin E deficiencies, indicating that selenium-vitamin E deficient chicks are not rendered scrobutic. Absorption experiments using ligated duodenal loops or oral doses indicated that dietary ascorbic acid promoted the enteric absorption of selenium but did not affect the absorption of vitamin E. These results support the hypothesis previously reported that factors which inhibit the oxidation of dietary selenium promote its absorption and, perhaps, its post-absorptive utilization in metabolically active components of the cell.

Animals↗

Studies on the enteric absorption of selenium in the chick using localized coccidial infections.

Studies were conducted to determine the primary loci of gastrointestinal absorption of inorganic selenium in the chick using radiotracer techniques and Eimeria sp. infections of known site specificity for the gastrointestinal tract. Results showed that coccidial infections in the anterior regions of the small intestine reduced selenium absorption and potentiated selenium deficiency among chicks fed critical levels of the mineral. Absorption experiments showed that selenium absorption was greatest in the duodenum and anterior ileum, although selenium was bound at least transiently to tissues in the gizzard and crop. It is concluded from these experiments that dietary inorganic selenium is absorbed primarily in the duodenum and anterior ileum. Factors such as enteric disease which disrupt the integrity of the anterior intestinal mucosa can, therefore, reduce the absorption of selenium and other nutrients absorbed in that region, resulting in a potentiation of nutritional deficiencies.

Animals↗

Pathology and histology of dietary tryptophan deficiency in broiler chicks.

The purpose of this experiment was to characterize a lesion of the rhamphotheca associated with tryptophan (TIRP) deficiency, search for other histological abnormalities,and determine whether bird size and housing conditions are contributing factors to these lesions. Day-old broiler chicks (Ross X Ross 308) were placed in either floor pens with fresh pine shavings or Petersime battery brooders with two pens of 10 chicks each per treatment. Broiler chicks from 0 to 21 days of age were fed adequate (0.24%) and deficient (0.09%) levels of TRP in diets based on corn, corn gluten meal, and gelatin. Separate groups of control chicks were pair fed daily with the deficient chicks. Deficient chicks grew less efficiently than did the pair-fed controls. Upon gross examination, a lesion of the maxillary rhamphotheca in the vicinity of the nares was observed in 61% of TRP-deficient birds housed in the battery and 13% of the birds housed in floor pens. A similar gross lesion was only observed in one control bird. These lesions were located along the upper portion of the beak between the nares and appeared as a crusty or scab-like area on gross examination, composed of detritus, heterophils, and plasma protein. Inflammation occasionally was observed at the dermoepidermal junction. The incidence of lesions was reduced in floor pens compared to battery brooders, but similarly sized birds did not exhibit the lesion. The number of lesions seen grossly and histologically in TRP-deficient birds, as compared to control birds, supports the hypothesis that TRP deficiency is the primary cause of these lesions around the nares of broilers. Secondary environmental factors, perhaps coprophagy, also influence the incidence of the lesion.

Animal Feed↗

Pathology and histopathology of gossypol toxicity in broiler chicks.

Two experiments were conducted to determine the toxicity, pathology, and histopathology of purified gossypol in broiler chicks. Gossypol was added to broiler feed at 0, 100, 200, and 400 mg/kg of feed in Experiment 1 and at 0, 800, and 1600 mg/kg of feed in Experiment 2. Day-old broiler chicks were fed these diets from 1 to 21 days in Experiment 1 and from 1 to 23 days in Experiment 2. In Experiment 1, body weight and feed intake at 21 days were not significantly affected by dietary gossypol. However, chicks fed gossypol at 400 mg/kg of feed had poor feed conversion ratio compared with the other treatment. Feed conversion ratios were 1.493, 1.564, 1.471, and 1.60 for chicks fed gossypol at 0, 100, 200, and 400 mg/kg of feed, respectively (Experiment 1). Chicks fed 400 mg/kg gossypol also had mild perivascular lymphoid aggregate formations and bilary hyperplasia in the liver. In Experiment 2, gossypol at 1600 mg/kg resulted in 28.1% mortality. Gossypol at 800 and 1600 mg/kg feed resulted in significant decreases in body weight and feed intake of chicks. The average body weights of 23-day-old chicks in Experiment 2 were 676, 224, and 111 g for 0, 800, and 1600 mg/kg gossypol, respectively. Feed conversion ratios of chicks fed 800 and 1600 mg/kg gossypol were significantly higher than those of chicks fed control diets (1.383 vs. 1.564 vs. 1.745 for 0, 800, and 1600 mg/kg gossypol, respectively). Plasma iron and hematocrit values were significantly reduced by gossypol at 800 and 1600 mg/kg of feed. Enlarged gallbladder was the only gross pathology symptom associated with gossypol levels. Severe cases of perivascular lymphoid aggregate formation, biliary hyperplasia, and hepatic cholestasis were observed in chicks fed 800 and 1600 mg/kg of gossypol in feed. No gossypol-related changes were observed in kidney tissues of chicks. These results show that gossypol is toxic to broiler chicks at high levels. This study also shows that histopathologic changes in liver due to gossypol also occur at levels lower than the levels that affect body weight.

Animal Feed↗