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Query: UNIPROT:Q4PNR5 (casein)
 17,724 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male weanling rats fed diets containing fermented and unfermented tannin-free sorghum meals naturally contaminated with traces of ochratoxin A, zearalenone, and an unidentified toxic substance developed anorexia. Mean changes in body weight over a 28-day feeding period for rats fed fermented and unfermented sorghum meal and ANCR casein diets of 8% protein were -2.8, +13.8, and +100.5 g, respectively. Rats fed fermented sorghum meal developed alopecia; hematological findings showed a decreased mean corpuscular volume, hypochromic microcytosis, balanced leukopenia, and hypoproteinuria . Histological findings showed testicular hypoplasia of the germinal epithelium and no mature spermatozoa. Necrosis and mineralization in Henle's loop were also observed. No damage was apparent to the liver, cerebellum, cerebrum, spleen, or adrenal glands.
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PMID:Toxic effects of fermented and unfermented sorghum meal diets naturally contaminated with mycotoxins. 623 60

The effect of anterior cingulate cortex lesions on dietary intake and adaptation of disproportionate amounts of amino acids was examined. Rats with bilateral electrolytic lesions in the anterior cingulate cortex and sham-operated rats were fed, in turn, amino acid basal, imbalanced or devoid diets involving threonine and isoleucine as the growth limiting amino acids, and then a low protein (6% casein) followed by a high protein (75% casein) diet. Lesions of the anterior cingulate cortex did not prevent the initial depression in food intake of the amino acid imbalanced diets, but shortened the duration of anorexia associated with dietary amino acid imbalances. Cingulate lesions did not influence the food intake of rats fed amino acid devoid diets. When switched from a low protein to a high protein diet, animals bearing lesions and sham-operated controls reduced markedly their initial food intake and adapted to the high protein diet in similar manner. It was concluded that the initial food intake depression associated with a dietary amino acid imbalance is a direct response to postingestive cues which influence food intake. Moreover, that the difference in adaptive intakes of the cingulate cortex lesioned animals who ingested a diet of imbalanced amino acids or of high protein, indicates that separate mechanisms act to control food intake of animals fed diets containing imbalanced amino acid mixtures or diets with excessive amounts of protein.
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PMID:Cingulate lesions and behavioral adaptation to amino acid imbalanced diets. 640 12

The effects of carbohydrate-deficient diets on the growth of the Walker carcinosarcoma 256 in rats and on the carcinostatic action of the glucose analogue 2-deoxyglucose were studied. All diets contained 13.0% casein with glucose levels as indicated and the balance of calories present as corn oil free fatty acids. The growth of the tumor was directly related to the glucose level in such diets; after 16 days rats fed 0.0, 1.5 and 4.5% glucose had tumors weighing 7.0, 11.1 and 13.3 g, respectively. The decrease in tumor weight was related to dietary glucose level rather than the anorexia produced by the diets low in glucose, as shown by the fact that tumors in rats fed 4.5% glucose were larger than rats fed 1.5% glucose even when the rats fed 4.5% glucose were pair-fed to the levels consumed by those fed 1.5% glucose. 2-Deoxyglucose (0.2%) also caused a reduction in tumor growth in a manner independent from the anorexia produced by its presence in the diet. This carcinostatic effect was potentiated by low glucose levels in the diets in the rats fed 4.5% glucose plus 0.2% 2-deoxyglucose had proportionally greater reductions in tumor weights due to the glucose analogue than did rats fed 20% glucose plus 0.2% 2-deoxyglucose.
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PMID:Effects of diets deficient in glucose and glucose precursors on the growth of the Walker carcinosarcoma 256 in rats. 649 63

A purified diet and two practical-type diets were each evaluated with supplemental biotin (1 mg/kg), without supplemental biotin, and with a biotin antagonist (freeze-dried egg white) for channel catfish (Ictalurus punctatus) over a 17-week feeding period. Omission of supplemental biotin from the casein-dextrin purified diet, with or without egg white, resulted in anorexia, reduced growth rate, lighter skin, hypersensitivity and reduced liver pyruvate carboxylase activity by this fish. Omission of supplemental biotin from either practical diet, one containing basically soybean meal and corn and another containing basically soybean meal, corn and menhaden fishmeal , caused none of these deficiency signs. The ratio of biotin to indigestible dry matter in feces was lower than that in the diet for all fish, indicating little or no synthesis of biotin by the intestinal microflora in channel catfish. Levels of total biotin, measured microbiologically, in the all-plant and in the plant- fishmeal diets were 0.37 and 0.33 mg/kg, respectively. These results indicate that practical diets for channel catfish made from the commonly used ingredients, soybean meal, corn and menhaden fishmeal , do not need supplemental biotin.
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PMID:Biotin supplementation of practical diets for channel catfish. 672 71

Purified casein diets with and without supplemental magnesium were fed to fingerling channel catfish (Ictalurus punctatus) in order to establish the essentially of this mineral. Fish fed the basal diet containing 0.004% magnesium developed deficiency signs such as poor growth, anorexia, sluggishness, muscle flaccidity and high mortality. After 3 weeks, two groups of fish fed the basal diet were converted to the supplemental diet containing 0.057% magnesium. Deficiency signs in these fish were alleviated almost immediately. In a second experiment, graded levels of magnesium sulfate were added to casein-based diets and fed to channel catfish fingerlings to determine their dietary requirement for magnesium. Results indicated that a minimum magnesium level of 0.04% of the dry diet was required to maintain normal growth, serum and bone magnesium levels in channel catfish fingerlings.
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PMID:Magnesium requirement of fingerling channel catfish and signs of magnesium deficiency. 708 46

Young chicks were used in a 16-d feeding study to evaluate the effects of excess dietary P on Mn utilization. The basal casein-dextrose diet (1.4 mg Mn/kg) was supplemented with 0, 3.5, 7.0, or 10.5 mg Mn/kg from MnSO4.H2O and was fed in the absence or presence of .8% excess dietary P (equal P contributions from KH2PO4 and NaH2PO4). Diets containing .8% excess P were also supplemented with .8% excess Ca (CaCO3) to keep the Ca:P ratio above 1:25 so as to prevent anorexia associated with excess dietary P per se. Both growth rate and total tibia Mn responded linearly (P < .01) to Mn supplementation in chicks fed the normal level of P, but those fed excess P responded erratically. Excess P did not affect growth or tibia Mn in chicks fed the basal diet, but birds fed diets with supplemental inorganic Mn grew slower (P < .01) and had lower (P < .01) quantities of Mn in tibia when excess P was supplemented. Manganese content in the tibia of chicks fed excess P was 55% of that in chicks fed an adequate level of P.
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PMID:Manganese utilization in the chick: effects of excess phosphorus on chicks fed manganese-deficient diets. 793 79

The minimum sodium requirement of growing kittens was measured using a 6 x 6 Latin square design. Twelve specific-pathogen-free short-hair growing kittens (six males, six females) were fed casein and lactalbumin-based purified diets supplemented with various levels of sodium (NaCI). Using six growing kittens (four males, two females), a sodium depletion and repletion study was conducted to define the variables associated with sodium deficiency. Sodium-deficient kittens exhibited anorexia, impaired growth, polydypsia, polyuria, hemoconcentration, reduced urinary sodium output and specific gravity, and elevated aldosterone concentration in plasma and output in urine. Plasma sodium concentration was not affected by dietary sodium intake. Urinary sodium output was positively related to (r = 0.818, P < 0.001), but fecal sodium loss was independent of sodium intake. These results suggest that sodium balance in kittens is essentially regulated by renal excretion. The recommended minimum sodium requirement of kittens for growth is 1.6 g Na/kg diet (energy density, 22 kJ ME/g diet), or 0.07 mg Na/kJ ME, or 34 mg Na x kg body wt(-1) x d(-1). A sodium requirement of adult cats for maintenance was estimated to be 21 mg Na x kg body wt(-1) x d(-1). These requirements are considerably greater than those recommended by the National Research Council in 1986.
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PMID:The minimum sodium requirement of growing kittens defined on the basis of plasma aldosterone concentration. 908 36

1. Glutathione concentrations in liver and lung fall when food intake or sulphur amino acid intake is inadequate. However, concentrations may be restored during inflammation, despite anorexia, provided that prior sulphur amino acid intake is adequate. 2. We studied the mechanisms of these changes by measuring the effect of sulphur amino acid and protein intake on hepatic glutathione synthesis and gamma-glutamylcysteine synthetase activity, hepatic and lung glutathione concentrations, glutathione reductase and glutathione peroxidase activities in young rats given an inflammatory challenge by intraperitoneal injection of tumour necrosis factor-alpha or endotoxin (lipopolysaccharide). 3. Diets containing 200 g of casein and 8 g of L-cysteine/kg (normal-protein diet), or 80 g of casein and 8 g of L-cysteine, or isonitrogenous amounts of L-methionine or L-alanine (low-protein diets) were fed ad libitum to young Wistar rats for 8 days. Dietary groups were subdivided into three: one subgroup continued feeding ad libitum, a second was given tumour necrosis factor or lipopolysaccharide and killed 24 h thereafter, while the third was pair-fed to the intakes of the second subgroup for 24 h before being killed. 4. Glutathione concentrations in liver and lung were reduced in rats fed the low-protein diet containing alanine, and in all dietary groups when food intake was restricted. The inflammatory challenges restored hepatic glutathione concentrations in all groups but the diet supplemented with alanine, which had an inadequate sulphur amino acid content. In lung, restoration occurred only in animals fed the normal-protein diet. 5. The activity of gamma-glutamylcysteine synthetase, which is rate limiting for glutathione synthesis, was unaffected by dietary or sulphur amino acid intake or by the inflammatory response. Substrate supply may therefore be a major determinant in glutathione synthesis in vivo. 6. Total hepatic glutathione synthesis was affected by food intake, the type and amount of sulphur amino acids in the diet and by inflammation. Total synthesis was 207, 137, 421 and 90 mumol/day for animals fed ad libitum the normal-protein diet, or low-protein diets supplemented with cysteine, methionine or alanine respectively, ad libitum. Pair-feeding resulted in values of 76, 31, 71, and 0 mumol/day respectively. After lipopolysaccharide injection, rates increased to 200, 117, 151 and 56 mumol/day respectively. 8. Reductase and peroxidase activities increased in liver and lung, when low-protein diets which contained supplemental methionine or alanine were consumed ad libitum. A reduction in food intake resulted in enzyme activity changes, which suggested that recycling of glutathione increased in lung and decreased in liver. Injection of tumour necrosis factor reversed this effect. 9. The restoration of glutathione concentrations in liver after an inflammatory challenge is closely associated with an enhanced rate of synthesis and increased recycling. The former is impaired when inadequate sulphur amino acid is consumed before the challenge. In lung, increased recycling of glutathione may help maintain concentrations when food intake is restricted, but not during inflammation.
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PMID:Dietary sulphur amino acid adequacy influences glutathione synthesis and glutathione-dependent enzymes during the inflammatory response to endotoxin and tumour necrosis factor-alpha in rats. 909 11

The sodium requirement of adult cats for maintenance was determined using a randomized block design of eight dietary sodium treatments (0.1, 0.4, 0.5, 0.66, 0.8, 1.2, 1.6 or 2.0 g Na/kg in a casein-lactalbumin-based purified diet) administered for periods of 4 wk. A total of 35 adult specific-pathogen-free domestic shorthaired cats (26 males and 9 females, 1.5-3 y of age) was given an equilibration diet (2 g Na/kg) for 14 d before assignment (or reassignment) to the treatments. A total of 12 cats (8 males, 4 females) was randomly assigned to the lowest six levels of sodium, and four cats to the highest two sodium levels. Cats consuming the diet containing 0.1 g Na/kg had significantly elevated aldosterone concentration in plasma, and packed cell volume. In addition, these cats exhibited anorexia, body weight loss, reduced urinary specific gravity and sodium excretion, and had a negative sodium balance. However, adult cats did not develop polydypsia and polyuria reported in sodium-deficient kittens. Cats given the diet containing 0.66 g Na/kg did not have an increased packed cell volume, but aldosterone concentration in the plasma was significantly elevated. However, cats given diets containing >/=0.8 g Na/kg had plasma aldosterone concentrations </=0.7 nmol/L (reference value for sodium-replete cats) and normal packed-cell volumes. A minimal sodium requirement of adult cats for maintenance of 0.8 g Na/kg diet (energy density = 22 kJ/g diet) or 0.4 mmol Na. kg body weight-1. d-1 is proposed.
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PMID:Sodium requirement of adult cats for maintenance based on plasma aldosterone concentration. 1002 21

We have conducted studies with juvenile yellow perch (Perca flavescens) over a period of 20 weeks to address the question of the interaction between water- and lipid-soluble antioxidant vitamins. Fish (2.25+/-0.14 g) were divided into twelve groups, and triplicate groups were fed one of four casein-based, semi-purified diets formulated to contain low or high vitamin E levels of either 5 or 160 mg/kg without or with vitamin C supplementation (250 mg/kg). Diets were designated as -C-E, -C+E, +C-E, or +C+E, respectively. The fish fed the +C+E diet showed significantly higher weight gain, feed intake, and feed efficiency than the groups fed vitamin C-deficient diets. Total ascorbate concentrations of liver were significantly higher in fish fed vitamin C-supplemented diets than in fish fed the vitamin C-deficient diet after 16 and 20 weeks. The liver alpha-tocopherol concentrations were increased by supplemental vitamin C in vitamin E-deficient dietary groups which indicates a sparing or regenerating effect of vitamin C on vitamin E. Fish fed vitamin C-deficient diets (-C-E and -C+E) exhibited severe deficiency symptoms, such as scoliosis, lens cataracts, anorexia, and haemorrhages. The cumulative mortality was significantly higher in the -C-E groups. The thiobarbituric acid-reactive substances value was significantly higher in blood plasma of fish fed a diet unsupplemented with both vitamins. The findings in the present study with yellow perch support the hypothesis that vitamin C regenerates and/or spares vitamin E in vivo.
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PMID:Interaction between vitamins C and E affects their tissue concentrations, growth, lipid oxidation, and deficiency symptoms in yellow perch (Perca flavescens). 1272 May 79


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