Egg shell quality and cholecalciferol metabolism in aged laying hens

Calcium-binding protein D28K (calbindin) synthesis, vitamin D metabolism and shell quality were investigated in young and aged laying hens fed diets containing either cholecalciferol (CC) or its 1-hydroxylated derivatives. Duodenal calbindin concentration was similar in the young and in the aged laying hens. Exogenous 1-hydroxylated CC derivatives increased duodenal calbindin concentration, regardless of age. Shell weight and shell density (mg/cm2) were significantly lower (P less than 0.01) in the aged than in the young hens. Egg shell weight and density tended to decrease along the clutch. The rate of decline was higher in aged than in young hens. Feeding aged hens a diet containing 5 micrograms 1,25-dihydroxycholecalciferol [1,25(OH)2CC] or 1 alpha-hydroxycholecalciferol per kilogram improved shell quality, slowed down the progressive reduction in shell quality during the clutch and increased culling and mortality. The results indicate a) that the capacity for expression of 1,25(OH)2D3 in the intestine is not altered by age and b) that prolonged feeding of 1-hydroxylated derivatives of vitamin D3 improves shell quality in aged laying hens and increases culling and mortality.     

Vitamin D metabolism in the hooded seal (Cystophora cristata)

Fish-eating mammals, such as seals, appear to ingest levels of vitamin D that are toxic to most mammals. To determine how seals cope with high vitamin D intakes, the metabolism of tritiated cholecalciferol ([3H]D3) was investigated in hooded seal (Cystophora cristata) pups during their postweaning fast and pups and adults consuming herring alone or supplemented with 400,000 iu D3 daily. [3H]D3 was metabolized to 25-[3H]OHD3 and 24,25-[3H](OH)2D3. 1,25-[3H](OH)2D3 was not detected, but plasma levels of 1,25-(OH)2D were similar to those in other mammals and were not affected by vitamin D intake. Plasma vitamin D, 25-OHD and 24,25-(OH)2D increased with vitamin D intake, but 25-OHD did not increase to the extent seen in other mammals. The supplemented seals showed no evidence of toxicity. Levels of 24,25-(OH)2D were higher in the unsupplemented seals (4 to 33 ng/mL) than reported in other mammals with similar 25-OHD levels and did not decrease with 25-OHD. High levels of 24,25-(OH)2D relative to 25-OHD have also been found in hooded seals in the wild. The half-lives of vitamin D, 25-OHD and 24,25-(OH)2D were shorter than those reported for most other mammals. Increased conversion of 25-OHD to 24,25-(OH)2D and a high capacity for vitamin D storage in their large blubber mass appeared to be factors in the resistance of seals to vitamin D toxicity.     

Effect of aluminum on performance and mineral metabolism in young chicks and laying hens

This study was performed to determine the long-term effects of dietary aluminum on egg production and reproductive parameters in the mature laying hen and on growth rate and feed efficiency in young chicks. The diets used in these studies were adequate in phosphorus and other essential nutrients. Aluminum added to constitute 0.30% of the diet severely depressed growth and reduced feed efficiency, bone ash and plasma phosphorus in male Ross x Leghorn chicks. At the same time, 0.15% added aluminum mildly depressed growth, feed efficiency and bone ash but had no effect on plasma phosphorus levels. The reduction in bone ash was relatively mild, and no clinical signs of rickets were observed. In laying hens, diets containing 0.15% added aluminum did not affect egg production, but 0.30% added aluminum reduced production significantly. Long-term exposure to aluminum increased percent shell in both groups receiving aluminum, whereas egg weight remained similar to that in controls. There were no changes in hatchability or bone ash associated with dietary aluminum. Although dietary aluminum influenced bone aluminum content, egg aluminum content was not affected. These studies indicate that dietary aluminum interferes with systems in addition to phosphorus metabolism.     

Receptor-mediated lipoprotein transport in laying hens

In laying hens, VLDL and vitellogenin (VTG) are secreted by the liver and eventually taken up by the growing oocyte via receptor-mediated endocytosis. Both macromolecules bind to the same receptor, termed the VLDL/VTG receptor, localized on the oocyte plasma membrane. Once taken up by the growing zygote, apolipoprotein B, the major protein constituent of VLDL, is proteolytically cleaved by a chicken-specific cathepsin-D. Systemic cholesterol homeostasis in the chicken is maintained by expressing a different apoprotein B-specific receptor in somatic cells, which in terms of its function is very similar to the mammalian LDL receptor. The phenotype of the Restricted Ovulator hen, characterized by hereditary hyperlipidemia and the absence of egg laying, was identified as a lack of expression of functional VLDL/VTG receptors in the oocytes without affecting somatic apoprotein B receptors.     

Vitamin D receptor (VDR) knockout mice reveal VDR-independent regulation of intestinal calcium absorption and ECaC2 and calbindin D9k mRNA

To study the role of calbindin D(9k) (CaBP) and epithelial calcium channel ECaC2 in intestinal calcium (Ca) absorption, vitamin D receptor knockout (KO) and wild-type (WT) mice were fed either 0.5% Ca or a 2.0% Ca rescue diet starting at 21 d of age. Ca absorption and parameters involved in this process were measured at 60 or 90 d of age. Compared with WT, KO mice fed the 0.5% Ca diet had higher plasma parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], and lower plasma Ca and insulin-like growth factor-I (IGF-I). Duodenal Ca absorption (% Ca absorbed) in KO mice was reduced 71% relative to WT mice and was associated with 55% lower CaBP mRNA, 47% lower CaBP protein and 95% lower ECaC2 mRNA levels. Compared with WT mice, the percentage of Ca absorbed in KO mice fed the 0.5% Ca diet was inappropriately low for the level of duodenal CaBP. The 2% Ca rescue diet normalized plasma Ca, prevented osteomalacia, increased growth and plasma IGF-I levels, but did not normalize plasma PTH or 1,25(OH)(2)D(3) in KO mice. In addition, the relationship between CaBP protein and the percentage of Ca absorbed was normalized, whereas ECaC2 mRNA fell to near zero. Our data demonstrate that higher CaBP levels do not ensure high rates of duodenal Ca absorption and that transcellular Ca absorption can occur even when ECaC2 gene expression is very low. In addition, our data suggest that the 2% Ca diet promotes a vitamin D receptor-independent anabolic effect on bone formation and calcium absorption, leading to improved calcium balance even in the presence of high PTH levels.     

Effect of dietary tung oil on the growth and lipid metabolism of laying hens

The influence of dietary tung oil, containing a high level of alpha-eleostearic acid (cis-9, trans-11, trans-13-octadecatrienoic acid, EA) on growth, egg production, and lipid and fatty acid compositions in tissues and egg yolks of laying hens was studied in White Leghorn hens. Forty-week-old hens were divided into three groups of eight birds each and fed diets containing 0, 0.5, or 1.0% tung oil for 6 wk. The average body weight, feed consumption, rate of egg production, and weights of eggs and yolks were not affected. The weight of adipose tissue was remarkably small in hens fed tung oil, whereas the yolk lipid content did not change. Triglyceride level in heart and adipose tissue decreased in hens fed tung oil, and the level of linolenic acid (C18:3) in all tissues was decreased. Alpha-EA was not almost deposited in the tissues and egg yolk of hens fed tung oil, but conjugated linoleic acid (CLA) was detected in all tissues and egg yolks. The level of CLA in the tissues was significantly higher with increased dietary tung oil. The order of CLA level in tissue lipids was adipose tissue>liver>heart>breast muscle. Especially, the level of CLA in the lipids of adipose tissue and egg yolks of hens fed 1.0% tung oil was 2.0% of the total fatty acid. These results supposed that dietary tung oil affected the lipid metabolism of laying hens and could modify the lipid and fatty acid composition in tissues and eggs.     

Plasma vitamin A composition and retinol-binding protein concentration during egg formation in laying hens

Blood plasma vitamin A composition (retinol, retinyl ester) and retinol-binding protein (RBP) were determined in three phases (empty; soft- and hard egg) of the egg formation period in laying hens. The retinyl ester level remained in the range of 6 to 11% of the total plasma vitamin A concentration during egg formation. The retinol and RBP increased significantly during the time of soft period. The molar ratio between retinol and RBP ranged between 0.72-0.77. The increase of retinol and RBP may be caused by the sexual steroid effect for satisfying the retinoid needs of the ovarium and shell gland (avian uterus).     

Vitamin D metabolism in magnesium deficient chicks

To determine if alterations in vitamin D metabolism are associated with the development of hypocalcemia in magnesium (Mg) deficiency, we measured plasma Mg, calcium (Ca), phosphorus (P) and vitamin D metabolites in growing chicks pair-fed diets adequate (1000ppm) or low (130ppm) in Mg for up to 15 days. A third group received a low Ca (0.2%) diet adequate in Mg and served as a positive control group in which the classical response to hypocalcemia was demonstrated. A progressive decline in plasma Mg in the Mg deficient chicks was associated with progressive and severe hypocalcemia. There was no rise in plasma 1,25-dihydroxycholecalcifetol (DHCC) in response to hypocalcemia in the Mg deficient chicks. In contrast, chicks fed low dietary Ca with adequate Mg exhibited a 3-fold elevation in circulating 1,25-DHCC and maintained plasma calcium slightly below that of control animals. The failure of the Mg deficient chicks to increase 1,25-DHCC production in response to hypocalcemia was not associated with inadequate circulating 25-hydroxycholecalciferol or increased plasma 24,25-DHCC. 1α-hydroxylase activity, measured in isolated renal tubules, was not elevated in the Mg deficient chicks, compared to controls. A significant correlation between plasma 1,25-DHCC and 1α-hydroxylase activity suggested that metabolic turnover of 1,25-DHCC was not significantly altered by Mg deficiency. The data suggest that the progression of hypocalcemia during Mg deficiency may be related to insufficient production of 1,25-DHCC in response to the prevailing hypocalcemia.     

Differential response of calcium transport systems in laying hens to exogenous and endogenous changes in vitamin D status.

Changes in intestinal calcium absorption, calcium deposition into egg shell, and intestinal, renal and uterine calcium-binding protein (CaBP) in laying hens were related to changes in 25 hydroxycholecalciferol-1-hydroxylase activity (1-hydroxylase), or to the supplementation of 1alpha-hydroxycholecalciferol (1alpha-OH-CC). The onset of egg production resulted in an increased kidney 1-hydroxylase activity and intestinal and uterine CaBP. Renal concentrations of CaBP remained unchanged. Intestinal calcium and phosphorus absorption, during the period of egg shell formation, and duodenal calcium-binding protein (CaBP), were higher in 1alpha-OH-CC-fed than in cholecalciferol-fed hens. Renal or uterine CaBP and calcium deposition into the egg shell did not fluctuate with the vitamin D source or concentration. 1alpha-OH-CC injection into non-laying Nicarbazinfed hens resulted in an increase in intestinal but not renal or uterine CaBP concentrations. It is suggested that (a) CaBP in various organs responded independently to the same stimuli; and (b) calcium deposition into egg shell and uterine CaBP level are not related to kidney 1-hydroxylase activity or concentration of 1,25 dihydroxycholecalciferol.     

Toxicity of high dietary levels of DDT in laying hens

Summary White Leghorn hens were fed diets containing 0, 300, 600, or 1200 ppm technical grade DDT for three 28-day periods. The 1200 ppm diet caused tremors and 33% mortality in the final period, but no gross toxicity symptoms were seen in birds fed the other diets. Egg production was decreased during the third period by 600 or 1200 ppm. Egg weight was decreased during the third period by 600 or 1200 ppm. Egg weight was decreased during the last two periods by 1200 ppm. Shell thickness was decreased in all three periods by feeding 600 or 1200 ppm DDT. Dietary DDT caused no change that could be detected by shell beta backscatter. Shell weight as a percent of total egg weight was decreased by 600 or 1200 ppm DDT.     

噻苯哒唑及其代谢产物在蛋鸡体内的残留分布及消除研究

目的探讨噻苯哒唑及其代谢物5-羟基噻苯哒唑在蛋鸡体内和鸡蛋中的残留分布及消除规律。方法选用30只健康蛋鸡进行试验,每天每只蛋鸡经口喂饲噻苯哒唑100mg,连续给药5天,分别于停药后第1天、第3天、第5天和第7天采集鸡蛋以及肝脏、肌肉、脂肪和心脏等组织制备组织匀浆。样品经乙腈提取,MCX固相萃取柱富集净化,超高效液相-串联质谱法测定噻苯哒唑及其代谢物的残留量。结果蛋鸡经口喂饲噻苯哒唑后,主要组织匀浆中5-羟基噻苯哒唑的含量显著高于噻苯哒唑,鸡蛋中两种药物的残留浓度最高。停药第一天时,组织中的残留水平(噻苯哒唑及5-羟基噻苯哒唑的浓度之和)顺序为肝脏>心脏>肌肉>脂肪。鸡蛋中噻苯哒唑的休药期约为7天。结论初步获得了噻苯哒唑及其代谢产物在蛋鸡组织中的残留水平及消除规律。     

Calcium metabolism, intestinal calcium-binding protein, and bone growth of rats fed high protein diets

The rat was used as a model for investigating the mechanism by which the consumption of high diets causes calciuria. Using a combined balance and kinetics study, calcium (Ca) metabolism was studied in 56-day old male rats which had been consuming a control (18% casein) or a high protein (36% casein) diet for 2, 14, or 28 days. Urine Ca was significantly increased to 1.7 mg/day and 1.1 mg/day in rats which consumed the high protein diet for 2 or 14 days respectively. After 29 days of consuming the high protein diet, urinary Ca excretion was 0.7 mg/day, the same as that of controls. No other criteria of calcium metabolism were significantly affected by the high protein intakes. Intestinal calcium-binding protein activity was not affected by consumption of the 36% casein diet for 7 days, nor was bone mineralization after consumption of this diet for 32 days. Since the rat excretes a low percentage of dietary Ca via the urinary route, it is not a useful model for studying Ca kinetics in protein-induced calciuria.     

Vitamin D and 1,25(OH)2D Regulation of T cells

Vitamin D is a direct and indirect regulator of T cells. The mechanisms by which vitamin D directly regulates T cells are reviewed and new primary data on the effects of 1,25 dihydroxyvitamin D (1,25(OH)₂D) on human invariant natural killer (iNK)T cells is presented. The in vivo effects of vitamin D on murine T cells include inhibition of T cell proliferation, inhibition of IFN-γ, IL-17 and induction of IL-4. Experiments in mice demonstrate that the effectiveness of 1,25(OH)₂D requires NKT cells, IL-10, the IL-10R and IL-4. Comparisons of mouse and human T cells show that 1,25(OH)₂D inhibits IL-17 and IFN-γ, and induces T regulatory cells and IL-4. IL-4 was induced by 1,25(OH)₂D in mouse and human iNKT cells. Activation for 72h was required for optimal expression of the vitamin D receptor (VDR) in human and mouse T and iNKT cells. In addition, T cells are potential autocrine sources of 1,25(OH)₂D but again only 48–72h after activation. Together the data support the late effects of vitamin D on diseases like inflammatory bowel disease and multiple sclerosis where reducing IL-17 and IFN-γ, while inducing IL-4 and IL-10, would be beneficial.