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A series of experiments was conducted to test the hypothesis that vitamin D utilization may not be as efficient in chicks with tibial dyschondroplasia (TD). The basal diet contained 1.0% Ca and 0.45% available P with no supplemental cholecalciferol (D3). Chicks from low TD (LTD) and high TD (HTD) selected lines were fed diets supplemented with various levels of vitamin D compounds and examined for rickets and TD. When chicks were fed a D3-deficient diet containing only 1.25 micrograms/kg added D3, HTD chicks had a greater incidence of severe rickets than LTD chicks (P < 0.05). The LTD chicks did not exhibit TD when fed a diet containing adequate (20 micrograms/kg) D3. The LTD chicks fed a diet supplemented with 5 micrograms/kg D3, however, had 22% incidence of TD. When HTD chicks were fed diets supplemented with 5 micrograms/kg D3 [control diet that meets NRC (1994) requirement for D3], 20 micrograms/kg D3, 5 micrograms/kg 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] or the combination of both D3 (20 micrograms/kg) and 1,25-(OH)2D3 (5 micrograms/ kg), TD incidence was highest in HTD chicks fed the control diet. When HTD chicks were fed diets with an increased dietary level of 1,25-(OH)2D3 (10 micrograms/kg) further reduction of TD incidence (P < 0.05) occurred. A potentially toxic level (Soares et al., 1983) of 1,25-(OH)2D3 (15 micrograms/kg) fed to HTD chicks resulted in still greater suppression of incidence of TD even though growth and feed intake in HTD chicks was greater than those of LTD chicks. It is concluded that the development of TD in HTD chicks is associated with subnormal ability to metabolize vitamin D.

Osteopontin (OPN) gene expression and alkaline phosphatase activity were evaluated in the epiphyseal growth plates of normal chickens and in diet-induced tibial dyschdroplasia (TD)-afflicted chickens. In the normal growth plate, OPN gene was expressed by a) cells of the subperichondrial zone surrounding the articular cartilage, b) a narrow layer of hypertrophic chondrocytes at the hypertrophic zone, and c) lower hypertrophic chondrocytes at the zone of matrix calcification and endochondral bone formation. The latter two layers were separated by OPN-negative chondrocytes. Osteopontin gene was not expressed throughout the zone of articular cartilage in the nonhypertrophic or upper hypertrophic portions of the growth plate cartilage. Only at sites of calcification of the lower hypertrophic zone was the expression of the OPN gene associated with alkaline phosphatase activity. In all TD lesions, regardless of the induction procedure, the layer of chondrocytes of the lower hypertrophic zone expressing the OPN gene and the layer of OPN-negative cells separating the two areas of OPN-expressing cells were grossly enlarged. This resulted in a wide discontinuity between the chondrocytes of the lower hypertrophic zone expressing the OPN gene and the cells expressing the OPN gene that are associated with mineralization. In TD, no alkaline phosphatase activity was detected within the growth plate cartilage, but normal OPN gene expression was observed at the subperichondrium zone and at the zone of endochondral bone formation. The results of this study suggest that in the epiphyseal growth plate, OPN expression is not restricted to sites of bone calcification.

A CHOLINE deficiency is readily produced in chicks by feeding a diet low in choline or certain choline precursors. The effect of choline deficiency in laying hens, however, is less clear. McCollum et al. (1912) fed a diet containing 70 parts ground polished rice previously extracted with hot alcohol and 30 parts of dried skimmed milk to laying hens and found that more lecithin was present in eggs produced by these hens than had been consumed in the diet. Therefore, these investigators concluded that large amounts of lecithin were synthesized by laying hens. Abbott and DeMasters (1940), using a diet similar to McCollum’s supplemented with other vitamins, found that addition of choline to this basal diet increased egg production, prevented weight loss, and reduced liver fat. When diets have been studied which were low in methionine and vitamin B12, good responses were obtained from the addition of choline to diets…

HIGGINS, Richert and Westerfeld (1956) observed normal development in chicks which received a purified casein diet containing approximately 0.02 mg. molybdenum per kg. of diet. An apparent molybdenum deficiency, however, was produced by feeding sodium tungstate. Tungstate feeding decreased growth rate, xanthine dehydrogenase activity and uric acid excretion, all of which were reversed by the addition of molybdenum to the diet. Reid et al. (1956) reported that chicks and turkey poults responded to additional dietary molybdenum when fed a purified diet containing isolated soybean protein. Further results by Kurnick et al. (1957) and Reid et al. (1957) indicated that tissue xanthine dehydrogenase activity as well as growth rate was increased by molybdenum supplementation of the basal diet. Using practical and purified diets, Teekel and Watts (1959) observed no beneficial effect from molybdenum supplementation when the chicks came from dams which received a regular diet. However, when the dams received a …

EARLY experiments by Titus (1932), Insko, Lyons and Martin (1938) and Lyons, Insko and Martin (1938) failed to show zinc to be a dietary essential for the chick. More recently, Mehring, Brumbaugh and Titus (1956) observed no beneficial effect upon growth of chicks from increasing the amount of zinc consumed from 42 to 820 mg. of zinc per kg. of diet. In studies on perosis, Wilgus, Norris and Heuser (1937), found that zinc as well as manganese had a beneficial effect upon the incidence of perosis, but under the conditions of their experiments manganese was shown to be the primary deficiency. Therefore, it was not until 1957, as a result of studies by O’Dell and Savage, that a true zinc deficiency was recognized in the chick. Edwards, Young and Gillis (1958), Moeller and Scott (1958), Morrison and Sarett (1958), Patrick (1958), and Roberson and Schaible (1958) have confirmed the original…

INTRODUCTION JUKES (1940) reported that choline is essential for the prevention of perosis in the chick. Further studies by Jukes and Welch (1942), Almquist and Grau (1944), Jukes, Olson and Dornbush (1945), and Jukes and Olson (1945) indicated that the intact choline molecule per se is responsible for the antiperotic properties of this substance. Betaine and other sources of labile methyl groups were ineffective in preventing perosis unless fed in combination with precursors of choline, such as monomethylethanolamine or dimethylethanolamine. However, little is known concerning the metabolic role of choline in preventing perosis. Since recent experiments in our laboratory have dealt with attempts to ascertain the role of choline in bone formation, a report by Miller et al. (1958) was of considerable interest. It was observed that the oral administration of diethylstilbestrol to choline-deficient rats protected them against death and produced certain lipotropic effects. This report is concerned with experiments …

Miller and Denton (1959) and Davies et al. (1960) reported that inorganic sulfate was effective in counteracting the toxic effects of supplying chicks with excess dietary molybdenum. The former investigators fed a diet composed of practical ingredients, including 35% of soybean oil meal, while the latter fed a purified diet containing isolated soybean protein. The addition of large quantities of sulfate ion to these diets in the absence of molybdenum did not affect growth. In contrast in experiments conducted at this laboratory with chicks using a purified diet containing casein as the protein source, marked growth depression was observed by feeding high levels of sulfate ion in attempts to induce molybdenum deficiency. The basal diet used in these experiments is given in Table 1. The mineral mixture in the diet supplied 0.23 to 0.41 percent inorganic sulfate. When sulfate ion was added to the diet, the calcium, sodium and potassium …