Dos Santos, Tiago Tedeschi;Srinongkote, S.;Bedford, M.R.;Walk, C.L.
Asian-Australasian Journal of Animal Sciences
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v.26
no.2
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pp.227-232
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2013
Phytate is not only an unavailable source of phosphorus (P) for broilers but it also acts as an anti-nutrient, reducing protein and mineral absorption, increasing endogenous losses and reducing broiler performance. The objective of this study was to investigate the anti-nutritional effects of phytate by including high levels of phytase in diets not severely limited in available P. A total of 768 male Arbor Acres broilers were distributed in six treatments of eight replicate pens of 16 birds each consisting of a positive control diet (PC), positive control with 500 FTU/kg phytase, negative control (NC) diet with lower available P and calcium (Ca) levels and the same NC diet with 500, 1,000 or 1,500 FTU/kg phytase. Body weight gain (BWG), feed intake (FI), feed conversion ratio (FCR) and mortality were determined at 21 and 35 d of age while foot ash was determined in four birds per pen at 21 d of age. FI, FCR and foot ash where not affected by the lower mineral diets at 21 d of age nor by the enzyme inclusion but broilers fed lower Ca and available P diets had lower BWG. At 35 d of age no difference was observed between broilers fed the positive or NC diets but broilers fed 500, 1,000 and 1,500 FTU/kg on top of the NC diet had better FCR than broilers fed the positive control diet. When compared to birds fed a diet adequate in P, birds fed the same diet included with 500, 1,000 and 1,500 FTU/kg of phytase in marginally deficient available P and Ca diets had an improvement of performance. These results support the concept that hydrolysing phytate and reducing the anti-nutritional effects of phytate improves bird performance on marginally deficient diets that were not covering the P requirement of birds.
Experiments were conducted with chicks and pigs to determine whether the sparing effects of cobalt (Co) or nickel (Ni) on zinc (Zn) nutrition were due to an improved Zn availability. They included a Zn balance study with New Hampshire X Leghorn cross chicks, a $^{65}Zn$ absorption study with Ancona chicks and a $^{65}Zn$ balance study with pigs. The basal diet was a corn-soybean type diet high in calcium. In the Zn balance study with New Hampshire X Leghorn cross chicks, Zn retention percentages for basal, + 54 ppm Ni or + 54 ppm Co were 39.4, 40.4 and 48.3, respectively. In the $^{65}Zn$ absorption study with chicks, adding these levels of Ni or Co to the basal diet increased $^{65}Zn$ absorption from 12.8% to 14.0% and 15.1%, respectively. Supplemental Ni and Co increased the proportion of body $^{65}Zn$ found in liver and bone. With the pig experiment, $^{65}Zn$ retention percentages for basal, +54 ppm Co and + 60 ppm Zn groups were 20.0, 26.7 and 12.2, respectively; while Zn retention values (mg) in the body were 29.5, 45.1 and 60.5, respectively. In addition, supplemental Co increased $^{65}Zn$ concentration in the blood, liver, kidney and duodenum. These studies showed that supplementation of the basal diet with Co resulted in increased absorption of dietary Zn in chicks and pigs. The effect of Ni in chicks was less than that of Co. The ability of supplemental Co and to a lesser extent of Ni to improve weight gain as well as reduce other Zn-deficient signs in both species fed a practical corn-soybean type diet high in in calcium can be explained, at least in part by an associated increase in Zn absorption. The possible mechanism involved in these effects are discussed.
This study examined the effects of excess intake of calcium(Ca) and iron(Fe) supplements on iron bioavailability, liver and kidney functions in anemic model rats. Seven-week-old female rats were first fed and Fe-deficient diet for ten weeks, and then fed one of nine experimental diets for an additional eight weeks, containing three levels of Ca, normal (0.5%) or high(1.5%) or excess (2.5%) and three levels of Fe, normal(35ppm) or high(210 ppm) or excess(350ppm). In anemic model rats, serum Fe, total iron binding capacity(TIBC), hemogolin(Hb), hematocrit(Hct) and liver Fe contents were significantly decreased. Apparent Fe absorption significantly increased with increasing dietary Fe levels, and decreased with increasing dietary Ca levels. serum Fe concentration significantly increased in rats fed a high- and excess-Fe diet, and decreased in rats fed a excess-Ca diet. TIBC was decreawed in rats fed a excess-Ca diet, and transferrin saturation(%) increased in rats fed ahigh- and excess-Fe diet. Hb and Hct were decreased in rats fed an excess-Ca diet regardless of dietary Fe levels. Fe and thiobarbituric acid reactin gsubstance(TBARS) Contents of liver significantly increased in rats fed a high- and excess0-Fe diet, and decreased in rats fed a high- and excess-Ca diet. Fe content of the spleen showed similar results. Urinary creatinine and GFR increased in rats fed an excess-Ca diet regardless of dietary Fe levels. GOT, GPT and LDH were not significantly affected by dietary Ca and Fe levels. These results suggest that excess intake of Fe may increase liver Fe deposits and TBARS, and excess intake of Ca may decrease Fe bioavailability and kidney function leading to potential health problems in anemic model rats.
This study examined the effects of excess intake of calcium (Ca) and iron (Fe) supplement on bone loss, nephrocalcinosis and renal function in osteoporotic model rats. Seven-week-old female rats were first fed a Ca-deficient diet for four weeks after ovariectomy operation, and then one of nine experimental diets for additional eight weeks, containing three levels of Ca, normal (0.5%) or high (1.5%) or excess (2.5%) and three levels of Fe, normal (35ppm) or high (210ppm) or excess (350ppm). The osteoporotic model rats showed a remarkable increase in body weight, serum alkaline phosphatase (ALP) and decrease in breaking force, Ca, P, Mg contents of femur. Serum Ca concentration was not significantly affected by dietary Ca and Fe levles. Liver Ca content increased in rats fed a high-and excess-Ca diet. Kidney Ca content and microscopic Ca deposition remarkably increased in osteoporotic model rats compared to control group, and showed a tendency to decrease in rats fed a excess-Ca diet. Breaking force of femur increased with increasing dietary Ca levels, but Ca, P contents of femur and serum ALP were not significantly affected by dietary Ca and Fe levels. Serum total protein decreased in rats fed a excess-Ca diet, BUN increased in rats fed a excess-Ca diet, while serum uric acid and creatinine were not significantly affected by dietary Ca levels. Urinary creatinine, GFR increased in rats fed a high-and excess-Ca, diet, and GFR was highest in rats fed a excess-Ca/excess-Fe diet. These results suggest that excess intake of Ca may increase breaking force of femur, but not increase mineral contents of femur, and decrease kidney function. Furthermore, excess intake of Fe and Ca concurrently may aggravate kidney function leading to potential health problems in ovariectomized osteoporotic model rats.
In the clinical state of vitamin D deficiency, it is possible that associated phosphate depletion, parathyroid hormone excess, and hypocalcemia may all depress the proximal tubular reabsorption of bicarbonate, in addition to abnormal skeletal modeling or remodeling, Although nutritional rickets is considered a rare disease in developed countries nowadays, cases of vitamin D deficient rickets caused by various unhealthy lifestyles such as insufficient exposure to sunlight, breast feeding infants without giving vitamin D supplements, unbalanced vegetarian diets of breast feeding mothers, low-birth weight, and maternal deficiency of vitamin D or calcium are increasing. Here, we present the case of an 8 month old girl, who was completely breastfed without any weaning diet or infant vitamin supplements. She visited our emergency room with hypocalcemic seizure and subsequently was diagnosed with vitamin D deficient rickets accompanied by overt bone changes and proximal renal lobular acidosis. After intravenous(IV) and oral calcium replacement therapy(IV calcium gluconate injection 1 mEq/kg/day for 6 days, 2 mEq/kg/day for 4 days followed by oral calcium gluconate administration 4 g/day for 3 days) with vitamin D supplement(Alfacalcidol 0.5 mcg/day) during admission, serum calcium level was normalized with clinical improvement. Oral sodium bicarbonate(0.6 g/day) was administered from the $2^{nd}$ hospital day for 2 weeks, which normalized the serum bicarbonate(measured by $tCO_2$) level. Calcium and vitamin D replacement were continued for 2 weeks and 3 months each. After discontinuing medications, follow up laboratory findings showed good maintenance of serum calcium, alkaline phosphate and bicarbonate levels with complete improvement of bone X-ray findings.
Purpose: To explore the influence of S100 calcium binding protein A4 (S100A4) knockout (KO) on methionine-choline-deficient (MCD) diet-induced non-alcoholic fatty liver disease (NAFLD) in mice. Materials and Methods: S100A4 KO mice (n=20) and their wild-type (WT) counterparts (n=20) were randomly divided into KO/MCD, Ko/methionine-choline-sufficient (MCS), WT/MCD, and WT/MCS groups. After 8 weeks of feeding, blood lipid and liver function-related indexes were measured. HE, Oil Red O, and Masson stainings were used to observe the changes of liver histopathology. Additionally, expressions of S100A4 and proinflammatory and profibrogenic cytokines were detected by qRT-PCR and Western blot, while hepatocyte apoptosis was revealed by TUNEL staining. Results: Serum levels of aminotransferase, aspartate aminotransferase, triglyceride, and total cholesterol in mice were increased after 8-week MCD feeding, and hepatocytes performed varying balloon-like changes with increased inflammatory cell infiltration and collagen fibers; however, these effects were improved in mice of KO/MCD group. Meanwhile, total NAFLD activity scores and fibrosis were lower compared to WT+MCD group. Compared to WT/MCS group, S100A4 expression in liver tissue of WT/MCD group was enhanced. The expression of proinflammatory ($TGF-{\alpha}$, $IL-1{\beta}$, IL-6) and profibrogenic cytokines ($TGF-{\beta}1$, COL1A1, ${\alpha}-SMA$) in MCD-induced NAFLD mice were increased, as well as apoptotic index (AI). For MCD group, the expressions of proinflammatory and profibrogenic cytokines and AI in KO mice were lower than those of WT mice. Conclusion: S100A4 was detected to be upregulated in NAFLD, while S100A4 KO alleviated liver fibrosis and inflammation, in addition to inhibiting hepatocyte apoptosis.
A reduced NaCl intake for the general population of the world has been recommended to reduce the overall blood pressure level and hence to reduce the overall incidence of cardiovascular disease. A high NaCl diet convincingly contributes to elevated arterial pressure in humans and animal models of hypertension. Among individuals there is considerable variability of blood pressure responsiveness to NaCl intake. In normotensive as well as hypertensive subjects, blood pressure can be judged to be salt sensitivity (SS) when observed to vary directly and substantially with the net intake of NaCl. The prevalence of SS in normotensive adults in the U.S. ranges from 15% to 42% and in hypertensive adults from 28% to 74%. SS is a risk factor for hypertension and may be an important marker in the identification of children for hypertension prevention programs. High NaCl intakes produce expansion of the extracellular fluid volume and thus increase blood pressure. Nonchloride salts of sodium does not expand the extracellular fluid volume and does not alter blood pressure. Blood pressure response to NaCl may be modified by other components of the diet. Low dietary intakes of potassium or calcium augment NaCl-induced increases of blood pressure. Conversely, high dietary intakes of potassium or calcium attenuate NaCl-induced hypertension. A greater intakes of potassium or calcium may prevent or delay the occurrence of hypertension. SS occurs when dietary potassium is even marginally deficient but is dose-dependently suppressed when dietary potassium is increased within its normal range. Orally administered KHCO$_3$, abundant in fruits and vegetates, but not KCl has a calcium-retaining effect which may contributed to its reversal of pressor effect of dietary NaCl. Since nutrients other than NaCl also affect blood pressure levels, a reduced NaCl intake should be only one component of a nutritional strategy to lower blood pressure.
Bozkurt, Mehmet;Kucukyilmaz, Kamil;Catli, Abdullah Ugur;Cinar, Mustafa;Cabuk, Metin;Bintas, Erol
Asian-Australasian Journal of Animal Sciences
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v.25
no.2
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pp.248-255
/
2012
Three levels of boron (0, 30, 60 ppm) were supplemented in practical corn-soybean based starter and grower diets, containing either adequate or inadequate Ca or P. A total of 1,800, 1-day-old sexed broiler chicks were assigned to six dietary treatments and fed with the experimental diets for 42 days. Boron improved the overall feed conversion ratio, but increased body weight only at 21 days of age (p<0.01). Boron decreased feed intake in the case of feeding on a diet deficient in Ca and P, and tended to increase feed intake when birds received a diet adequate in Ca and P, signifying significant boron by Ca-P interaction (p<0.01). Mortality was not influenced by boron (p>0.05). Dietary Ca and P deprivation reduced body weight and feed consumption significantly, but did not influence the feed conversion ratio and mortality (p>0.05). Serum Ca level, ALP and ALT activities were not influenced either by dietary Ca and P deficiency or boron supplementation. Serum P content increased with respect to boron at 30 ppm. Bone breakage strength was not affected by dietary variables. Tibia ash, Ca and P were increased in response to the supplementation diet with 30 ppm boron, whereas 60 ppm showed no effect in most cases. Accordingly, the dietary boron supplementation of 30 ppm significantly decreased fecal Ca and P excretion, while there was a numerical decline in the 60 ppm boron as compared to the 0 ppm boron group. Data presented herein indicated that boron, either at the 30 ppm or 60 ppm supplementation level, was effective in conversion of feed to body weight, whereas only boron at 30 ppm contributed to the mineralization of bone thereby augmenting more Ca and P while excreting less through faeces.
Lee, Kyoung Soon;Asante, Lydia S.;Chun, Sung Soo;Yun, Mi Eun
The Korean Journal of Community Living Science
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v.26
no.4
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pp.661-673
/
2015
This study examines the effects of a low-calorie raw juice diet on the level of serum ferritin in adults and analyzes nutrient intake from the diet. There were significant differences between juices; the highest calorie was provided by pear juice, highest crude protein, vitamin A, and vitamin B2 levels were from green Juice 1; and highest vitamin C and vitamin B1 levels were from fruit juices. The ratio of estimated energy requirements (EER) for the participants was 56.2% from the raw juice diet. The percentages of recommended intake (RI) from the raw juice diet of protein (57.9%), dietary fiber (19.1%), niacin (6.2%), calcium (0.1%), and magnesium (0.2%) were lower than 75%. However, those of RI of vitamin A, vitamin B1, vitamin B2, vitamin B6, and vitamin C were 1796.5%, 7481.7%, 1915.5%, 30858.7%, and 7500%, respectively, exceeding the tolerable upper intake level (UL) for vitamin A, vitamin B6, and vitamin C. There were significant decreases in weight, the body mass index (BMI), body fat mass, and skeletal muscle mass in males and females. After the diet program, serum iron and SOD (superoxide dismutase) showed significant decreases, whereas RBC, hemoglobin, hematocrit, and serum ferritin showed significant increases. There were negative correlations between serum ferritin and weight and between serum ferritin and skeletal muscle mass for all participants. There were negative correlations between serum ferritin and skeletal muscle mass for males and between serum ferritin and body fat mass for females. These results suggest that a raw juice diet can supplement a regular diet to prevent excess or deficient nutrient intake.
This study investigated the effect of dietary supplementation with phytase on growth performance, fecal excretion, and compost nutrition on broilers fed available phosphorus (avP)- and calcium (Ca)-deficient diets. A total of 750 one-day-old broiler chicks were randomly divided into five dietary groups having ten replications in a floor house. Diets of the groups were formulated with positive control (PC), negative control (NC; low avP and Ca), and NC supplemented with phytase levels; 500 (NC500), 1,000 (NC1000), and 1,500 FTU/kg (NC1500). A three-phase feeding program was used in the trial. Average daily gain (ADG) and average daily feed intake (ADFI) in the groups fed diets supplemented with phytase were significantly (p < 0.05) higher than those fed NC and the increase was equivalent to those fed PC. Serum levels of Ca and phosphorus (P) were higher (p < 0.05) in broilers fed NC1000 and NC1500 than in those fed NC. Interleukin (IL) level was the lowest in the group fed NC. Plasma myo-inositol (INS) concentrations in the NC1500 group were higher (p < 0.05) than PC, NC, and NC500 groups. Crude protein (CP) excretion was notably (p < 0.05) lower in the NC1500 group than in PC and NC groups. A lower (p < 0.05) concentration of P2O5 was observed in compost from the group fed NC1500 than the groups fed PC and NC. Accordingly, we suggest that phytase supplementation in lower avP and Ca levels of broiler diet can improve their productive performance and reduce environmental pollution.
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