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)

To study the defective transport mechanism of cystinuria, renal tubular reabsorption of lysine or arginine in normal and cystinuria subjects was investigated by increasing the filtered load employing intravenous amino acid infusion. In the normal group the amino acid reabsorption rose with increases of the filtered load and reached a maximum (Tm). In the cystinuria group the elevation of amino acid reabsorption was poor at low filtered loads and some of the reabsorption rates fell below zero, whereas the tubular transport proceeded at a normal rate with a great increase of the filtered load. This might be explained as follows: At low filtered loads the filtered amino acid in the tubular lumen in patients with cystinuria is not absorbed into the cell because of a transport defect of the luminal membrane of the tubular cell, causing a large amount of urinary amino acid excretion. At high filtered loads the accumulated intraluminal amino acid permeates the tubular cell by a passive diffusion and is transported to the capillary across the intact basolateral membrane, which in turn only brings about a small urinary loss of amino acid. The infusion of lysine or arginine depressed the percentage of tubular reabsorption of other dibasic amino acids in both groups. In the cystinuria group the percentage of the dibasic amino acid reabsorption dropped sharply with an initial load of the inhibitor, but no more depression of the percentage of reabsorption occurred with further loads of the inhibitor.
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PMID:Renal transport of lysine and arginine in cystinuria. 640 4

In a series of five trials, 680 crossbred pigs were fed isolysine diets in which high protein (13.8 to 16.0%) oats constituted 0, 20, 40 or 60% of the cereal portion. There was a linear depression in average daily gain (P less than .001) and average daily feed intake (P less than .005) with increasing level of oats, but feed/gain was unaffected (P less than .05) during the growing period from 22 to 46 kg. There were no significant differences in average daily gain during the finishing period from 46 to 102 kg; however, feed/gain increased linearly (P less than .01) with increasing level of oats in the diet. Increases in the percentage of oats in the cereal portion of the diet resulted in a linear (P less than .01) decrease in average daily gain and an increase (P less than .01) in feed/gain for the entire feeding period. We conclude that high protein-high lysine oats of the quality used in these trials can be included at up to 20% of the cereal portion of the diet without greatly affecting performance.
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PMID:Evaluation of high protein oats as a replacement for corn in diets fed to growing-finishing swine. 640 15

Feeding diets with 4% L-lysine to the chick produces an elevation of plasma lipids which does not occur when feeding an excess of any other amino acid. Experiments were conducted to determine whether lysine-induced hyperlipidemia is secondary to the antagonistic effect of lysine on arginine or to the anorexia which accompanies lysine feeding, and in addition, whether the lysine-induced hypercholesterolemia is affected by chick age. In all experiments gain and food intake were reduced by feeding chicks 4% lysine. Plasma cholesterol and triglyceride were elevated, but high-density-lipoprotein cholesterol, as a percentage of total, was reduced. Addition of dietary arginine up to 4% failed to reverse the depression in performance and elevation of plasma lipids. Pair-feeding the control diet to the amount consumed by lysine-fed chicks did not elevate plasma lipids above control levels. Thus, lysine-induced hyperlipidemia is not mediated by the antagonistic effect of lysine on arginine nor by the effect of lysine on food intake. The high-lysine diet prevented the normal decline in plasma cholesterol expected with advancing age of chicks. Preliminary results suggested that excess lysine stimulated cholesterol biosynthesis.
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PMID:Effect of excess dietary lysine on plasma lipids of the chick. 641 75

Fifteen gravid, crossbred gilts were utilized in an experiment to measure the effect of five isonitrogenous dietary treatments (12% crude protein, sorghum-soybean meal; sorghum; sorghum + lysine; sorghum + threonine; sorghum + lysine + threonine) on N balance, colostrum composition and plasma constituents (protein, urea N and IgG). All gilts were fed a standard corn-soybean meal diet from breeding until switched to the sorghum basal diet, on d 60 of gestation. Treatment diets were imposed at d 70. Nitrogen retention, measured between d 103 and 113 of gestation, was improved (P less than .002) by lysine addition. Nitrogen retention was similar (P greater than .10) for gilts fed either the 12% crude protein, sorghum-soybean meal diet or the lysine + threonine-supplemented diet. Plasma protein levels at farrowing were depressed (P less than .06) in those gilts fed sorghum diets without supplemental lysine and plasma urea N was elevated (P less than .10). Plasma protein and plasma urea N were not affected by threonine supplementation (P greater than .10). In contrast, the depression of plasma IgG was ameliorated (P less than .03) by threonine and unaffected by lysine supplementation. These results confirm the hypothesis that lysine is the first limiting amino acid in sorghum protein for gravid gilts as determined by N retention but indicate that threonine is likely the first limiting amino acid for the production of the specific protein, IgG.
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PMID:Effect of lysine and threonine supplementation of sorghum gestation diets on nitrogen balance and plasma constituents in first-litter gilts. 642 57

The effect of excess amino acids on utilization of the most limiting amino acid was investigated via restricted feeding. Lysine- and threonine-deficient amino acid mixtures were incorporated into diets for young growing rats to provide 75 or 85% of the NRC requirement of the limiting amino acid in combination with zero or 50% of relative excess of the nonlimiting amino acids. The amount of food offered was equalized within treatment groups and increased according to the intake of the group with the lowest rate of consumption. Because of differences in the amount of diet refused, total food intakes were not identical. At equal percentage of the NRC requirement, threonine- and lysine-deficient amino acid mixtures supported equal body weight, dry matter, lipid and ash gains. However, crude protein retention was greater when the threonine-deficient amino acid mixture was fed. The maximum depression in performance due to 50% of amino acid excess with restricted feeding was much less than the maximum decrease previously observed in the ad libitum feeding situation. This supports the conclusion that changes in voluntary food intake are the major effectors of depressed growth due to excess amino acids. These results raise serious concern over the usefulness of amino acid requirements and the applicability of the current system of chemical scores to evaluate protein quality.
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PMID:The effect of amino acid excess on utilization by the rat of the limiting amino acid--lysine and threonine at equalized food intakes. 643 11

The interaction of methionine or lysine with lead in the diet of chicks was studied. In experiment 1, lead acetate to supply 0 or 1000 ppm lead was added to a diet that was either deficient in the total sulfur-containing amino acid (TSAA) content (62% of the requirement) or supplemented with DL-methionine to provide 100% of the requirement (NRC, 1977). Supplementing the 0 ppm lead diet with methionine improved body weight gain. Dietary addition of 1000 ppm lead significantly decreased body weight gain; however, supplemental methionine partially alleviated the lead-induced growth depression (methionine X lead interaction was significant). Liver glutathione levels were markedly increased by supplemental methionine and also by lead but no methionine X lead interaction was detected. In experiment 2, the interaction between an essential non-sulfur-containing amino acid, lysine, and dietary lead was investigated. Two levels of lead, 0 or 1000 ppm, were fed in diets either deficient or adequate in lysine (85 or 100% of the requirement, respectively). Addition of lysine to the lysine-deficient basal diet increased growth. The magnitude of the lead-induced growth depression was not affected by dietary lysine content. The lysine level of the diet did not influence the liver glutathione concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary methionine and lysine on the toxicity of ingested lead acetate in the chick. 643 52

Serum amino acid (AA) levels were determined for 18 cholecystectomy patients who had preserved and immediately utilized G-I function for absorption of 3,000 kcal/day elemental diet. Ten were given 132 gm AA/day; eight were given only 66 gm AA/day. Historical controls were 27 comparable patients who had received conventional hypocaloric intravenous (IV) regimens. Unfed patients' branched chain AAs (BCAAs) + TYR were depressed initially, then rebounded by day 3 or 4. Their glucogenic AAs were still depressed after 72 hours. Complete restoration of the basal pattern required five to ten days. Fully nourished patients maintained basal levels of all AAs on day 1. Every AA rose above basal, some with statistical significance as early as day 2. Moderately fed patients had BCAA depression, but for only 24 hours. LEU, ILE, VAL, TYR, MET, ASP, LYS, and ARG had already returned to basal levels on day 2, while the remaining AAs were much less depressed than in the unfed controls. All fed patients were discharged uneventfully 24-48 hours postcholecystectomy. The positive protein balance and elevated AA levels correlate with enhanced wound healing, host sepsis resistance, and shortened hospitalization.
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PMID:Elevation of postoperative plasma amino acid concentrations by immediate full enteral nutrition. 643 8

A quantitative literature review has been used as the basis of an empirical simulation model of the responses in food intake and egg output of laying hens to temperature, light pattern, light intensity, feeding system type, crude protein, methionine, lysine and metabolisable energy. The financial consequences are considered, by the calculation of gross margin of egg value minus food cost. Response to protein intake in an optimal environment is taken as the first limiting factor. Depressions below the maximum are calculated for sub-optimal environments. The model was tested against a sample of flocks for which detailed records were available, and found to give realistic answers. A FORTRAN program was written which calculates egg output and food intake by 4-week production periods, permitting the user to examine the effects of management changes made during lay. Shortened versions of the model, based on annual values have been written for a programmable calculator.
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PMID:A model of egg production. 647 77

The effects of several dietary factors on the anorexigenic response to monensin in chicks fed corn-soybean meal diets varying in crude protein (CP) were investigated. In Trial 1, crossbred chicks (New Hampshire X Columbia) were fed a 16% CP diet with or without 160 mg/kg monensin and/or .53% potassium carbonate in a 2 X 2 factorial design. Monensin supplementation caused a 24.5% growth depression, and potassium carbonate had no effect on the monensin-induced depression. Trials 2 and 3 were designed to evaluate the effects of dietary energy level on the monensin response in commercial broiler chicks fed diets containing 24, 20, or 16% CP. As CP level was decreased, the depression in performance from 121 mg/kg monensin increased. Increasing the energy concentration of the 24 and 20% CP diets to that of the 16% CP diet had no consistent effect on the response of chicks to monensin. Trial 4 was conducted to determine the influence of amino acid (AA) supplementation on the monensin response in broiler chicks fed a low-protein diet. Supplementation of a 16% CP diet with an AA mixture (3% glutamic acid plus essential AA equal to the 24% CP diet) improved growth performance markedly. Deletion of methionine, arginine, and lysine from the AA mixture yielded performance well below that of chicks fed the unsupplemented 16% CP diet, indicating a severe AA imbalance. Monensin supplementation at 121 mg/kg caused a much greater growth depression in chicks fed 16% CP or 16% CP plus the complete AA mixture than in those fed 24% CP or the AA-imbalanced 16% protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of dietary electrolyte balance, energy, and amino acid supplementation on the monensin response in chicks fed diets varying in protein content. 653 32

The ability of amino acids inhibitory of lysine transport into brain slices to induce lysine imbalance was determined by feeding wheat gluten or casein diets with additions of such amino acids. Lysine transport was only moderately inhibited by amino acids; the most effective were basic amino acids or mixtures of indispensable (IAA) or branched chain amino acid (BCAA). Only mild depressions in growth and food intake occurred during a 10-day period when male, 60--65 g rats of the Sprague-Dawley strain were fed lysine-limiting, 18% wheat gluten diets with additions of these amino acids. The effects were prevented by added lysine. Rats allowed a choice between the lysine-imbalanced or non-protein diets selected the imbalanced, wheat gluten diets (in severe imbalances rats will choose the non-protein diet). Growth depression, prevented by added lysine, occurred in rats fed a 6% casein diet supplemented with IAA; individual amino acids were ineffective. Growth depressions also occurred when rats were fed a basal diet containing 6% case in + 5% of an equimolar mixture of nine IAA and supplemented with arginine or more IAA; BCAA were less effective. Additional lysine completely prevented the growth depressions, but growth of rats fed the diets containing arginine and BCAA was greater than that of those fed the extra IAA. It is difficult to induce a severe lysine imbalance; this is consistent with the failure of amino acids to cause under our conditions strong inhibition of lysine transport into brain.
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PMID:Induction of lysine imbalance in rats: relation to competition for lysine transport into the brain in vitro. 678 81


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