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)

The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.
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PMID:Effect of ACTH-stimulated glucocorticoid hypersecretion on the serum concentrations of thyroxine-binding globulin, thyroxine, triiodothyronine, reverse triiodothyronine and on the TSH-response to TRH. 23

Growth of Escherichia coli AB 2271 under threonine or isoleucine deficiency leads to a depression of the threonyl-tRNA synthetase and isoleucyl-tRNA synthetase respectively. During this amino-acid-limited growth the concentrations of isoaccepting fractions of the cognate tRNA species were changed, as demonstrated by their altered reversed-phase-5 chromatograms. But, in addition, the profiles of the isoacceptors of all other tRNA species investigated, i.e. of tRNAsLeu, tRNAsSer and tRNAsArg were also altered. This means that, if there is a correlation between regulation of the level of an aminoacyl-tRNA synthetase and its cognate isoaccepting tRNAs, it is superimposed by the effect of amino acid limitation upon the concentration of all isoaccepting tRNAs. So far drastic changes in profiles of isoaccepting tRNAs have only been observed under unbalanced growth in relaxed cells or during treatment with antibiotics. Here we demonstrate that similar heavy alterations in patterns of isoaccepting tRNAs occur in a proven stringent E. coli strain growing exponentially under amino acid limitation. Thus the observed changes in the profiles of isoaccepting tRNAs during amino acid limitation signal a meaningful biological function of those newly or increasingly occurring isoaccepting tRNAs. During the growth under amino acid limitation the total acceptor activity of eight investigated tRNA species, however, stayed unchanged, except that under threonine-limited growth the total amount of tRNAIle was reduced to about half and that of tRNAGlu increased; both tRNA species of these isoacceptors are known [30,31] as spacers between ribosomal RNAs.
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PMID:Alteration of the intracellular concentration of aminoacyl-tRNA synthetases and isoaccepting tRNAs during amino-acid limited growth in Escherichia coli. 34 70

The ability of low protein diets containing small neutral, dispensable amino acids to induce threonine imbalance has been examined. Diets containing amino acids which compete for threonine transport in vitro (serine, alanine, alpha-amino-n-butyrate) caused depressions of growth and food intake which could be corrected to varying degrees by adding threonine to the diet. Large neutral, indispensable amino acids, moderately inhibitory of threonine transport, also induced the imbalance. Some amino acids that had little or no effect on threonine transport in vitro (acidic amino acids and proline) did not cause growth and food intake depressions. Other non-inhibitory amino acids (arginine and lysine) caused growth depressions which were not satisfactorily corrected by additional threonine alone, but were prevented by supplements of all the indispensable amino acids including threonine. Ornithine which was also not inhibitory of threonine transport was an exception. It induced a moderate growth depression which was corrected by additional threonine. Similar studies showed that histidine or tryptophan imbalance could be induced by feeding diets containing only those large neutral amino acids which compete for histidine or tryptophan transport in vitro. These experiments show that, based on the results of transport competition experiments, it is generally possible to devise amino acid supplements which can induce a dietary imbalance of a given amino acid.
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PMID:Induction of threonine imbalance by dispensable amino acids: relation to competition for amino acid transport into brain. 43 Feb 32

Bilateral double electrolytic overlapping lesions were placed in dorsal-lateral hippocampus of male 230 g rats, and their food intake responses to the ingestion of diets containing disproportionate amounts of amino acids were examined. Rats with such lesions and intact control rats maintained their normal intakes of the 6% casein basal diet or a threonine basal amino acid diet postoperatively. However, they exhibited marked initial food intake depression, similar to that of intact rats, when fed the threonine imbalanced amino acid diet. Also, animals with lesions in certain areas of the dorsal-lateral hippocampus showed facilitated adaptation to the amino acid imbalanced diet. Similar severe reduction in food intake with relative lack of adaptation were observed in both the intact controls and rats with hippocampal lesions when fed amino acid diets completely devoid of threonine. Initial food intake of rats with hippocampal lesions was inhibited drastically as was the case with the intact controls when fed a 75% casein high protein diet. All rats, either intact or lesioned, showed similar slow adaptation patterns with the prolonged ingestion of the high protein diet. The initial food intake responses and facilitated adaptation of the animals bearing lesions in certain areas of the hippocampus suggest that such areas are not crucially involved in the inhibition of food intake of rats fed disproportionate amounts of dietary amino acids. Rather, such areas of lesions in the hippocampus may play a role in a system governing the behavioral adaptation of the intake of amino acid imbalanced diets but not of diets containing amino acids in general excess. This would also indicate that different mechanisms control the intake of amino acid imbalanced diets and diets containing amino acids in excess.
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PMID:Effects of hippocampal lesions on adaptive intake of diets with disproportionate amounts of amino acids. 51 2

Young male crossbred chicks were fed crystalline amino acid diets containing excess L-methionine or DL-homocysteine to evaluate factors causing methionine toxicity. Chicks were fed diets containing graded levels of excess methionine from 0% to 2.0%. Rate of gain was reduced at all levels of excess methionine, but the magnitude of depression was greater between 1% and 2% than between 0% and 1% excess methionine. Methionine accumulated in plasma of birds fed excess methionine, but plasma levels of homocysteine, cystathionine and cystine remained essentially unchanged. Spleen iron levels increased linearly and blood hemoglobin decreased linearly when chicks were fed diets containing greater than 1% excess methionine, a level equivalent to about 3 times the chicks' requirement. Chicks fed 1.36% homocysteine had reduced gain and gain:feed values, but spleen iron and hemoglobin levels were unchanged. 3-Methylthiopropionate, a possible metabolite in a proposed alternate pathway, caused a precipitous increase in spleen iron levels. Various methyl sources (betaine, choline, methyl acetate) when fed in excess failed to increase spleen iron levels. Methyl mercaptan and methyl mercaptoacetate likewise did not result in an increase in spleen iron deposition. Both the hemosiderosis condition and the reduced food utilization caused by excess methionine were reversed by supplemental glycine plus threonine.
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PMID:Factors affecting methionine toxicity and its alleviation in the chick. 66 Feb 99

The ilv 1 gene in S. cerevisiae codes for a regulatory protein involved in depression of the ilv 2 and ilv 3 genes as well as a biosynthetic enzyme, threonine deaminase. 2. The ilv 1 gene does not autogenously regulate its catalytic product threonine deaninase. 3. Regulation of the ilv 2 and ilv 3 gene products involve different aporepressors than regulation of the ilv 1 gene product. 4. The ilv I multifunctional gene in S. cerevisiae may be a duplication and fusion of a bacterial like ilv 1 gene where ilv 1 catalytic and regulatory function have been differentially conserved.
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PMID:Regulation of the ilv 1 multifunctional gene in Saccharomyces cerevisiae. 76 33

The object of this study was to determine the effects of individual amino acid supplements on the development of tyrosine toxicity in growing rats fed 10% casein containing 5% tyrosine. Each amino acid was added at levels equivalent to its content in 20% casein. Supplement of methionine to the high tyrosine diet partially alleviated both growth depression and pathological lesions. Threonine and cystine had a somewhat beneficial effect, but the single addition of other amino acids was not effective. Besides, some amino acids enhanced the severity of the toxicity even more. The effects of methionine supplementation were highest at 0.66 to 1.32% levels (equivalent to the methionine content in 20 to 40% casein). By the supplement of both 0.66% methionine and 0.90% threonine to the high tyrosine diet, growth was significantly improved and toxic lesions were completely prevented. It was confirmed that the counteracting effects to the toxicity, caused by the extra addition of protein (casein) to rats fed a high tyrosine-low protein diet, were mainly attributed to the effectiveness of the methionine and threonine, i.e., first-and second-limiting amino acids, respectively, contained in it.
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PMID:Effect of individual amino acid supplements on the toxicity of excess tyrosine in rats. 101 Oct 50

Plasma albumin levels were measured in partially hepatectomized, sham operated and control rats. The levels fell in both the partially hepatectomized and sham operated groups; while the latter group returned to normal within a few days, the low plasma albumin in the partially hepatectomized animals was sustained. Albumin synthesis rates in the isolated perfused rat liver were measured in the three groups of animals at varying intervals after partial hepatectomy. There was a significant depression of albumin synthesis rate in terms of both liver and whole animal weights when compared to the sham operated and control animals. This depression was almost completely reversed by the addition of arginine, asparagine, isoleucine, leucine, lysine, methionine, phenylalanine, proline, threonine, tryptophan and valine added together to 10 times their normal plasma concentrations. The addition of hydrocortisone had no effect on the albumin synthesis rate after partial hepatectomy. Studies in vivo in the three groups of animals (partially hepatectomized, sham operated and control animals) revealed a fall in the albumin catabolic rate after partial hepatectomy coinciding with the fall in the albumin synthesis rate. An hypothesis whereby the amino acids may have their stimulatory effect is proposed.
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PMID:Albumin synthesis and catabolism following partial hepatectomy in the rat. The effects of amino acids and adrenocortical steroids on albumin synthesis after partial hepatectomy. 115 98

Studies were conducted to evaluate the involvement of food intake in the lysine-arginine antagonism. Diets were formulated to compensate for the metabolic consequences of excess dietary lysine; induction of renal arginase activity, depression of heptic glycine transamidinase, and urinary losses of arginine. This was accomplished by inclusion of creatine in the basal diet, use of a moderate excess of lysine that did not increase urinary arginine excretion, and addition of the arginase depressors, alpha-aminoisobutyric acid (AIB) and L-threonine, to diets containing excess lysine. When chicks were fed diets containing excess lysine ad libitum, growth and efficiency of arginine retention were reduced. Supplementation of the diets with AIB and threonine markedly reduced the growth depression and restored efficiency of arginine utilization. When chicks were force-fed the diet containing excess lysine, growth was depressed, and body composition was altered. Inclusion of AIB and threonine in the diet containing excess lysine resulted in growth and body composition equivalent to levels of force-fed controls. In a second experiment the basal diet and basal supplemented with AIB and threonine were pair-fed to lysine-supplemented diets containing AIB and threonine. Body weight gains and body composition of all groups were similar. In other experiments, food intake increased within 24 hours (P less than 0.05) and probably within 12 hours (P less than 0.10) after removal of excess lysine from the diet. It is concluded that a portion of the lysine-arginine antagonism is due to a primary effect of lysine on regulation of food intake.
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PMID:Involvement of food intake in the lysine-arginine antagonism in chicks. 115 27

Several assays with young chicks fed crystalline amino acid diets were conducted to investigate the effects of supplemental glycine, serine, threonine, arginine, or adenine on the growth depression resulting from consumption of excess methionine. Glycine was partially effective in alleviating the growth depression caused by excess methionine. The addition of threonine together with glycine improved performance still further. Efficiency of food utilization for weight gain was greater in birds fed the methionine-imbalanced diet supplemented with glycine and threonine than in those fed the control diet. Supplemental glycine, threonine, or adenine, but not arginine, was effective in ameliorating the hypoglycemia resulting from consumption of excess methionine. The rate of oxidation of a tracer dose of threonine was increased markedly by feeding 1.25% excess methionine. This was reflected in a 20% depression in threonine utilization for weight gain as measured by slope ratio. The data suggest that both threonine and glycine are antagonized by consumption of excess methionine.
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PMID:Methionine toxicity in the chick: nutritional and metabolic implications. 115 32


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