Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A significant impairment in growth rate, food efficiency and weight of the gastrocnemius muscle was observed in rats fed a raw legume as the source of protein compared to casein-fed animals. No appreciable differences in chemical composition of the carcass were found. The source of dietary protein did not influence the ratio protein/DNA, DNA concentration or protein-synthesizing capacity (RNA/protein). The slower weight gain of animals fed the legume diet was attributed to a lower muscle protein synthesis, mediated by a depression of muscle RNA activity (grams protein synthesized/gram RNA) rather than changes in myofibrillar protein breakdown. In contrast liver protein synthesis appeared to be slightly increased in the legume-fed animals.
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PMID:Response of muscle, liver and whole-body protein turnover to two different sources of protein in growing rats. 243 91

The effects of methyl-group acceptors such as glycine, guanidinoacetic acid, and nicotinamide on cholesterol metabolism and phosphatidylcholine(PC) biosynthesis were investigated with rats fed a 25% casein diet containing cholesterol with or without methionine supplement. The effect of ethanolamine, an indirect methyl-group acceptor via phosphatidylethanolamine(PE) formation, was also compared with those of methyl-group acceptors. The methyl-group acceptors and ethanolamine decreased or tended to decrease plasma total cholesterol level when added to the 25% casein diet. These compounds also significantly depressed the methionine-induced enhancement of plasma cholesterol level. The activity of PE N-methyltransferase was decreased by the addition of glycine, guanidinoacetic acid, and nicotinamide, but not ethanolamine, to the reaction mixture when assayed using the postmitochondrial fraction of liver homogenate, suggesting that PE N-methyltransferase activity can be depressed by glycine N-methyltransferase, guanidinoacetic acid N-methyltransferase, and nicotinamide N-methyltransferase systems. The PE N-methyltransferase activity in liver microsomes, however, did not decrease in response to the dietary addition of methyl-group acceptors. The in vitro incorporation of [CH3-14C]methionine into PC of liver slices was also significantly inhibited by the addition of glycine and nicotinamide, but not guanidinoacetic acid and ethanolamine, to the incubation medium. It is suggested that methyl-group acceptors can decrease plasma cholesterol level at least in part through the depression of PC biosynthesis via PE N-methylation pathway, and that the mechanism for the plasma cholesterol-lowering effect of ethanolamine is different from that of methyl-group acceptors.
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PMID:Effects of methyl-group acceptors on the regulation of plasma cholesterol level in rats fed high cholesterol diets. 253 19

The chemotactic locomotion of peritoneal macrophages in vitro was measured in the presence of supernatant fluid from 27 different tumour cell lines. All the tumour-derived cells tested caused profound depression of macrophage chemotaxis towards the chemo-attractant casein. Conversely, supernates from rapidly dividing non-malignant cells uniformly failed to depress macrophage migration. This confirms the results of a previous investigation and provides further evidence that malignant tumours depress the functions of the reticuloendothelial system of the host animal in vivo.
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PMID:Inhibition of macrophage chemotaxis by supernatant fluid from malignant cell lines. 285 68

Food intake, plasma and brain amino acid concentrations, liver amino acid catabolic enzyme activities, and whole-brain neurotransmitter and metabolite concentrations were measured in young rats adapted for 11 d to diets containing from 5 to 75% (in increments of 5%) casein. Food intake was depressed initially in rats fed diets containing 5, 10% or greater than 35% casein. For the duration of the experiment, food intakes of the groups fed the higher protein diets improved on successive days; the length and severity of the depression were proportional to the protein content of the diet fed. Rats fed low levels of protein grew poorly, and their food intake remained depressed. The gradual improvement in growth and food intake of rats fed diets containing more than 35% casein was accompanied by dramatic increases in the activities of serine-threonine dehydratase (SDH, EC 4.2.1.16) and glutamate-pyruvate aminotransferase (GPT, EC 2.6.1.1) in liver. The increase in amino acid catabolic activity was accompanied by decreases in the concentrations of most amino acids in plasma and brain. However, concentrations of branched-chain amino acids, in both plasma and brain, increased in direct proportion to the protein concentration of the diet fed. As a result of these reciprocal responses, the total concentration of indispensable amino acids in brain (IAA) was maintained within a narrow range of values, despite a sixfold range of protein intakes. Whole-brain concentrations of norepinephrine, dopamine and serotonin were not correlated with dietary protein concentration, total food intake or protein intake. Brain concentrations of homovanillic acid and 5-hydroxyindoleacetic acid were correlated inversely with protein intake and that of 3,4-dihydroxyphenylacetic acid was correlated directly with food intake. Protein intake appeared to be related to the animal's ability to maintain brain total IAA content between some upper and lower limits. Our results indicate that this was accomplished initially through downward adjustment of protein intake and subsequently through an increase in catabolic capacity for the amino acids.
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PMID:Adaptation of rats to diets containing different levels of protein: effects on food intake, plasma and brain amino acid concentrations and brain neurotransmitter metabolism. 285 80

This study evaluated the effect of prostaglandin I2 (PGI2) on fibronectin-mediated macrophage phagocytosis in vivo and in vitro. Phagocytosis measured in vivo in rats by the vascular clearance rate and hepatic localization gelatinized sheep erythrocytes was inhibited in a dose-dependent manner after intravenous administration of PGI2. Phagocytosis was assessed in vitro in terms of uptake of fibronectin-dependent gelatinized sheep erythrocytes by monolayers of casein-elicited rat peritoneal macrophages. Concentrations of 1 ng/ml PGI2 or greater resulted in inhibition of particle internalization but not attachment to macrophages. This inhibitory effect was enhanced by aminophylline, a phosphodiesterase inhibitor. PGI2 increased cAMP levels and these were further increased in the presence of aminophylline. These data indicate that PGI2 inhibits macrophage uptake of gelatinized particles and support the idea that this is mediated by increased intracellular levels of cyclic AMP. PGI2 should thus be considered a potential etiologic factor in the phagocytic depression observed in association with thrombosis.
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PMID:Influence of prostaglandin I2 on fibronectin-mediated phagocytosis in vivo and in vitro. 298 44

Three chick growth assays were conducted to investigate the effects of monensin on lysine and arginine utilization in crossbred chicks (New Hampshire X Columbian). Chicks were fed either a low lysine corn-sesame meal diet containing graded increments of crystalline lysine.HCl (Assay 1) or an arginine-deficient casein-dextrose diet (Assay 2) supplemented with graded levels of L-arginine.HCl in the presence or absence of supplemental monensin (121 mg/kg). Based upon analysis by slope-ratio methodology (i.e., gain regressed on supplemental amino acid intake), the efficiency of L-lysine or L-arginine utilization was found to be the same in both monensin-fed and control chicks. In Assay 3, effects of monensin on the lysine-arginine antagonism were studied. Chicks were fed an arginine-deficient casein-dextrose diet supplemented with 1 or 2% L-lysine.acetate in the presence or absence of supplemental monensin. Growth performance was depressed by feeding both levels of supplemental L-lysine.acetate. Monensin had no effect on the magnitude of the growth depression caused by supplemental lysine. These results support the view that neither lysine nor arginine utilization is impaired by feeding monensin.
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PMID:In vivo utilization of lysine and arginine in young chicks fed monensin. 313 6

Rats were trained to eat a 6% casein basal diet during a 3-hour period per day. They were then fed either the same 6% casein diet or a 44% casein diet for 3 hours. No food intake depression was observed in the rats eating 44% casein diet during the 3-hour period. Plasma ammonia and amino acids and brain amino acids were measured at 0, 4, 12 and 24 hours after presentation of the 6% or 44% casein diets. Plasma ammonia rose to 134 (p less than 0.01) and 110 micromolar (p less than 0.05) in the 44% casein fed rats at 4 and 12 hours, respectively, as compared to 67 and 53 micromolar, respectively, for the 6% casein fed rats. All plasma amino acid concentrations except methionine and glutamate were elevated (p less than 0.05) at 4 hours. In the brain, threonine, glutamine and tyrosine concentrations were elevated (p less than 0.05) at 4 hours after diet presentation. At 24 hours, valine, isoleucine, leucine, phenylalanine, and methionine concentrations were also elevated (p less than 0.05). Because intake of the 44% casein diet decreases the second day of its presentation, as noted in an earlier experiment, the increases in plasma ammonia and its possible entry into the brain as reflected by increased brain glutamine together with changes in amino acid concentrations should be considered collectively among possible metabolic signals affecting intake of high protein diets.
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PMID:Increase in plasma ammonia and amino acids when rats are fed a 44% casein diet. 320 Sep 19

To evaluate nutritional availability and chronic toxicity of KSeCN, female postweanling rats were fed casein-based diets plus 0.1, 0.5, 2.5, 5 and 10 mg Se/kg as KSeCN for 6 wk, or 0.1, 0.5 and 10 mg Se/kg as Na2SeO3. A control group was fed the basal diet (Se = 0.04 mg/kg) and one group was fed the basal diet plus 5 mg Se/L as KSeCN in the drinking water. There were no differences in weight gain and diet consumption among groups fed 2.5 mg Se/kg or less. At 5 and 10 mg Se/kg, rats showed depression in weight gain and diet consumption. After wk 6 there were no abnormalities of the major organs of rats fed 2.5 mg Se/kg or less. Spleen enlargement was observed at 5 and 10 mg Se/kg, and liver damage and kidney enlargement at 10 mg Se/kg. Se content in the blood, liver and kidney of rats fed KSeCN was generally somewhat lower than for those fed Na2SeO3 at the same levels. The availability of Se from KSeCN for glutathione peroxidase formation in blood, liver and kidney was comparable to that of Na2SeO3. Plasma thyroxine in groups fed 10 mg Se/kg was 40% of that in the control group, but was not altered at lower Se levels.
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PMID:Nutritional availability and chronic toxicity of selenocyanate in the rat. 337 36

Three experiments were conducted to evaluate the influence of dietary protein source on the monensin response in healthy chicks fed diets varying in CP. The interrelationship between dietary CP level and four different anticoccidial drugs was evaluated in a fourth experiment. The experiments were conducted from 8 to 21 or 22 days posthatching. In Experiment 1, crossbred chicks were fed corn-soybean meal (SBM) diets containing either 24 or 16% CP or casein-dextrose diets containing 20, 15, or 10% CP in the presence or absence of 160 mg/kg monensin. When CP level was decreased in the corn-SBM treatments, the resulting monensin-induced growth depression was greater. However, this interaction was not observed in chicks fed casein-dextrose diets. Experiments 2 and 3 were conducted to determine if the monensin-protein level interrelationship is influenced by the source of dietary soybean protein or by high levels of animal protein (AP). Monensin at 140 mg/kg produced a much greater growth depression at 16 than at 24% CP in chicks fed a corn-SBM diet, whereas amounts of monensin depression in chicks fed a corn-isolated soy protein diet were similar for both CP levels. As dietary protein was reduced from 24 to 16% in Experiment 3, 140 mg/kg monensin caused growth depressions of 10 and 40%, and 14 and 28%, respectively, in broiler chicks fed corn-SBM and corn-AP diets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Further investigation of the dietary protein level-monensin interrelationship in broiler chicks: influence of dietary protein source and type of anticoccidial drug. 340 44

Twenty-four Holstein cows (early postpartum) were used in a randomized complete block design with a 2 X 2 factorial arrangement of treatments to compare effects of nicotinic acid (niacin) and whole cottonseed. Cows were fed individually isonitrogenous complete mixed rations ad libitum, containing corn-soy concentrate, corn silage, chopped coastal bermudagrass hay, and either 1) 0% niacin and 0% whole cottonseed, 2) 0% niacin and 15% whole cottonseed, 3) .03% niacin and 0% whole cottonseed, or 4) .03% niacin and 15% whole cottonseed. Dry matter and energy consumption, actual milk yield, total milk solids, and milk fat yield were not affected by treatment. Either niacin or whole cottonseed increased milk fat percentage and 4% fat-corrected milk. Milk protein percentage and yield were higher with niacin supplementation but tended to be lower with cottonseed feeding. The milk protein depression with whole cottonseed was alleviated by niacin due to stimulation of mammary casein synthesis. Supplemental niacin tended to elevate glucose and insulin in blood plasma, but whole cottonseed tended to reduce these plasma components. Plasma urea nitrogen was higher in cows fed whole cottonseed. Plasma-free tryptophan tended to be slightly higher in cows receiving supplemental niacin.
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PMID:Influence of niacin and whole cottonseed on intake, milk yield and composition, and systemic responses of dairy cows. 355 22


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