Academic literature on the topic 'Catabolism of mammal amino acids'
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Journal articles on the topic "Catabolism of mammal amino acids"
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Робонен (Robonen), Елена (Elena) Вильямовна (Vil'yamovna), Надежда (Nadezhda) Петровна (Petrovna) Чернобровкина (Chernobrovkina), Оксана (Oksana) Васильевна (Vasil'evna) Чернышенко (Chernyshenko), Мария (Mariya) Игоревна (Igorevna) Зайцева (Zaytseva), Алексей (Aleksey) Рудольфович (Rudol'fovich) Унжаков (Unzhakov), and Анастасия (Anastasiya) Васильевна (Vasil'evna) Егорова (Egorova). "PERSPECTIVES OF WOOD-GREENERY BIOTECHNOLOGY ENRICHMENT WITH L-ARGININE AND INHIBITORS OF ITS CATABOLISM." chemistry of plant raw material, no. 1 (March 6, 2019): 23–37. http://dx.doi.org/10.14258/jcprm.2019014243.
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A promising source of L-arginine, as well as natural inhibitors of its catabolism enzymes, are plants. Free amino acids constitute a significant part of the water-soluble fraction of woody greenery of coniferous plants, including L-arginine. The biotechnology of L-arginine enrichment of coniferous woody greenery is developed by regulating nitrogen and boron support. The fact of a multiple increase in the pool of free L-arginine in needles suggests an increase in the level of enzyme inhibitors of its catabolism. Coniferous greens contain guanidine compounds, which are therapeutic agents for controlling the activity of nitric oxide synthases. L-arginine, one of the most universal amino acids in the metabolism of the animal body, in mammals is classified as a conditionally essential amino acid. The imbalance of the activities of the arginic and NO-synthase catabolism pathways of arginine, competing for the substrate, can lead to pathological consequences for the organism. Activation of inducible NO synthase or arginase reflects the type of inflammatory response in the development of specific diseases. In their treatment, the effectors controlling the activity of catabolism enzymes are considered as targets for pharmacological action. Examples of the use in folk medicine of extracts from some species of gymnosperms are given in the works of ethnomedical orientation. Analysis of the current state of studies of the metabolism of L-arginine in living organisms and its features in coniferous plants was carried out for the scientific substantiation of the prospects of obtaining enzymes for its metabolism of woody greens enriched with L-arginine and effector enzymes.
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Stewart, Gavin S., and Craig P. Smith. "Urea nitrogen salvage mechanisms and their relevance to ruminants, non-ruminants and man." Nutrition Research Reviews 18, no. 1 (June 2005): 49–62. http://dx.doi.org/10.1079/nrr200498.
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AbstractMaintaining a correct balance of N is essential for life. In mammals, the major sources of N in the diet are amino acids and peptides derived from ingested proteins. The immediate endproduct of mammalian protein catabolism is ammonia, which is toxic to cells if allowed to accumulate. Therefore, amino acids are broken down in the liver as part of the ornithine–urea cycle, which results in the formation of urea – a highly soluble, biochemically benign molecule. Mammals cannot break down urea, which is traditionally viewed as a simple waste product passed out in the urine. However, urea from the bloodstream can pass into the gastrointestinal tract, where bacteria expressing urease cleave urea into ammonia and carbon dioxide. The bacteria utilise the ammonia as an N source, producing amino acids and peptides necessary for growth. Interestingly, these microbial products can be reabsorbed back into the host mammalian circulation and used for synthetic processes. This entire process is known as ‘urea nitrogen salvaging’ (UNS). In this review we present evidence supporting a role for this process in mammals – including ruminants, non-ruminants and man. We also explore the possible mechanisms involved in UNS, including the role of specialised urea transporters.
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Teleni, E. "Catabolism and synthesis of amino acids in skeletal muscle: their significance in monogastric mammals and ruminants." Australian Journal of Agricultural Research 44, no. 3 (1993): 443. http://dx.doi.org/10.1071/ar9930443.
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The enhanced rate of synthesis and catabolism of amino acids in, and their release from, skeletal muscle, particularly during fasting, exercise and metabolic acidosis, highlight the integrative role of muscle in protein-energy metabolism. This review discusses aspects of such changes in muscles of monogastric mammals and ruminants. The glucose-alanine cycle, as it was originally proposed, has been well substantiated by studies using human and rat muscles. An alternative proposal, which suggested that other amino acids make a major contribution to the carbon skeleton of alanine synthesized in muscle, is less convincing, since some of the inhibitors and substrates used in relevant studies have been demonstrated to have multiple rather than specific effects. In the ruminant, the glucose-alanine cycle is quantitatively less significant than in human. The probable reason for this difference is the limited available pyruvate in ruminant muscle for transamination to alanine. This may be due to a lower carbon flux through the glycolytic pathway and/or to significant activity of the anaplerotic enzyme, pyruvate carboxylase. It is suggested that glutamine is the more important carrier of carbon and nitrogen out of skeletal muscle and that alanine may serve only as an ancillary vehicle to transport carbon and nitrogen when the availability of pyruvate for transamination in muscle is high. The more diverse role of glutamine (cf. alanine) in acid-base balance, as a respiratory fuel in the cells of the immune system and the epithelia of the small intestine, where it may also be converted to alanine for subsequent gluconeogenesis in the liver, is consistent with this suggestion.
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Matthews, Dwight E. "Review of Lysine Metabolism with a Focus on Humans." Journal of Nutrition 150, Supplement_1 (October 1, 2020): 2548S—2555S. http://dx.doi.org/10.1093/jn/nxaa224.
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ABSTRACT Lysine cannot be synthesized by most higher organisms and, therefore, is an indispensable amino acid (IAA) that must be consumed in adequate amounts to maintain protein synthesis. Although lysine is an abundant amino acid in body proteins, lysine is limited in abundance in many important food sources (e.g. grains). Older observations assigned importance to lysine because animals fed a lysine-deficient diet did not lose weight as fast as animals placed upon other IAA-deficient diets, leading to the theory that there may be a special pool of lysine or metabolites that could be converted to lysine. The first step in the lysine catabolic pathway is the formation of saccharopine and then 2-aminoadipic acid, processes that are mitochondrial. The catabolism of 2-aminoadipic acid proceeds via decarboxylation to a series of CoA esters ending in acetyl-CoA. In mammals, the liver appears to be the primary site of lysine catabolism. In humans, the metabolic and oxidative response of lysine to diets either restricted in protein or in lysine is consistent with what has been measured for other IAAs with isotopically labeled tracers. Intestinal microflora are known to metabolize urea to ammonia and scavenge nitrogen (N) for the synthesis of amino acids. Studies feeding 15N-ammonium chloride or 15N-urea to animals and to humans, demonstrate the appearance of 15N-lysine in gut microbial lysine and in host lysine. However, the amount of 15N-lysine transferred to the host is difficult to assess directly using current methods. It is important to understand the role of the gut microflora in human lysine metabolism, especially in conditions where dietary lysine intake may be limited, but better methods need to be devised.
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Herring, Cassandra M., Fuller W. Bazer, Gregory A. Johnson, and Guoyao Wu. "Impacts of maternal dietary protein intake on fetal survival, growth, and development." Experimental Biology and Medicine 243, no. 6 (February 22, 2018): 525–33. http://dx.doi.org/10.1177/1535370218758275.
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Maternal nutrition during gestation, especially dietary protein intake, is a key determinant in embryonic survival, growth, and development. Low maternal dietary protein intake can cause embryonic losses, intra-uterine growth restriction, and reduced postnatal growth due to a deficiency in specific amino acids that are important for cell metabolism and function. Of note, high maternal dietary protein intake can also result in intra-uterine growth restriction and embryonic death, due to amino acid excesses, as well as the toxicity of ammonia, homocysteine, and H2S that are generated from amino acid catabolism. Maternal protein nutrition has a pronounced impact on fetal programming and alters the expression of genes in the fetal genome. As a precursor to the synthesis of molecules (e.g. nitric oxide, polyamines, and creatine) with cell signaling and metabolic functions, L-arginine (Arg) is essential during pregnancy for growth and development of the conceptus. With inadequate maternal dietary protein intake, Arg and other important amino acids are deficient in mother and fetus. Dietary supplementation of Arg during gestation has been effective in improving embryonic survival and development of the conceptus in many species, including humans, pigs, sheep, mice, and rats. Both the balance among amino acids and their quantity are critical for healthy pregnancies and offspring. Impact statement This review aims at: highlighting adverse effects of elevated levels of ammonia in mother or fetus on embryonic/fetal survival, growth, and development; helping nutritionists and practitioners to understand the mechanisms whereby elevated levels of ammonia in mother or fetus results in embryonic/fetal death, growth restriction, and developmental abnormalities; and bringing, into the attention of nutritionists and practitioners, the problems of excess or inadequate dietary intake of protein or amino acids on pregnancy outcomes in animals and humans. The article provides new, effective means to improve embryonic/fetal survival and growth in mammals.
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Lobley, G. E. "Protein turnover—what does it mean for animal production?" Canadian Journal of Animal Science 83, no. 3 (September 1, 2003): 327–40. http://dx.doi.org/10.4141/a03-019.
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The dynamics of protein turnover confer great advantages for homeothermy, plasticity and metabolic function in mammals. The different roles played by the various organs have led to aspects of protein synthesis and degradation that aid the various functions performed. The so-called “non-productive” organs such as the gastro-intestinal tract and liver produce large quantities of export proteins that perform vital functions. Not all these proteins are recovered, however, and thus function can result in lowered net conversion of plant protein to animal products. The splanchnic tissues also oxidize essential amino acids (AA). For example, the gut catabolizes leucine, lysine and methionine, but not threonine and phenylalanine, as part of a complex interaction between AA supply and tissue metabolic activity. Losses by oxidation and endogenous secretions can markedly alter the pattern of absorbed AA. The fractional rates of extraction of total AA inflow to the liver are low and this allows short-term flexibility in controlling supply to peripheral tissues. Recent evidence suggests that the role of the liver in AA catabolism is more a response to non-use by other tissues rather than an immediate regulation of supply to the periphery. Neither arterial supply of AA nor the rate of transport into peripheral tissues limits protein gain, except when supply is very limited. Rather, control is probably exerted via hormone-nutrient interactions. Key words: Protein synthesis, amino acid, gastro-intestinal tract, liver, muscle, mammary gland
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Liu, Yingying, Fengna Li, Lingyun He, Bie Tan, Jinping Deng, Xiangfeng Kong, Yinghui Li, Meimei Geng, Yulong Yin, and Guoyao Wu. "Dietary protein intake affects expression of genes for lipid metabolism in porcine skeletal muscle in a genotype-dependent manner." British Journal of Nutrition 113, no. 7 (March 16, 2015): 1069–77. http://dx.doi.org/10.1017/s0007114514004310.
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Skeletal muscle is a major site for the oxidation of fatty acids (FA) in mammals, including humans. Using a swine model, we tested the hypothesis that dietary protein intake regulates the expression of key genes for lipid metabolism in skeletal muscle. A total of ninety-six barrows (forty-eight pure-bred Bama mini-pigs (fatty genotype) and forty-eight Landrace pigs (lean genotype)) were fed from 5 weeks of age to market weight. Pigs of fatty or lean genotype were randomly assigned to one of two dietary treatments (low- or adequate-protein diet), with twenty-four individually fed pigs per treatment. Our data showed that dietary protein levels affected the expression of genes involved in the anabolism and catabolism of lipids in the longissimus dorsi and biceps femoris muscles in a genotype-dependent manner. Specifically, Bama mini-pigs had more intramuscular fat, SFA and MUFA, as well as elevated mRNA expression levels of lipogenic genes, compared with Landrace pigs. In contrast, Bama mini-pigs had lower mRNA expression levels of lipolytic genes than Landrace pigs fed an adequate-protein diet in the growing phase. These data are consistent with higher white-fat deposition in Bama mini-pigs than in Landrace pigs. In conclusion, adequate provision of dietary protein (amino acids) plays an important role in regulating the expression of key lipogenic genes, and the growth of white adipose tissue, in a genotype- and tissue-specific manner. These findings have important implications for developing novel dietary strategies in pig production.
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MacIver, Bryce, Craig P. Smith, Warren G. Hill, and Mark L. Zeidel. "Functional characterization of mouse urea transporters UT-A2 and UT-A3 expressed in purified Xenopus laevis oocyte plasma membranes." American Journal of Physiology-Renal Physiology 294, no. 4 (April 2008): F956—F964. http://dx.doi.org/10.1152/ajprenal.00229.2007.
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Urea is a small solute synthesized by many terrestrial organisms as part of the catabolism of protein. In mammals it is transported across cellular membranes by specific urea transporter (UT) proteins that are the products of two separate, but closely related genes, referred to as UT-A and UT-B. Three major UT-A isoforms are found in the kidney, namely UT-A1, UT-A2, and UT-A3. UT-A2 is found in the thin, descending limb of the loop of Henle, whereas UT-A1 and UT-A3 are concentrated in the inner medullary collecting duct. UT-A2 and UT-A3 effectively represent two halves of the whole UT-A gene and, when joined together by 73 hydrophilic amino acids, constitute UT-A1. A biophysical characterization of mouse UT-A2 and UT-A3 was undertaken by expression in Xenopus laevis oocytes and subsequent preparation of highly enriched plasma membrane vesicles for use in stopped-flow fluorometry. Both isoforms were found to be highly specific for urea, and did not permeate water, ammonia, or other molecules closely related to urea (formamide, acetamide, methylurea, and dimethylurea). Single transporter flux rates of 46,000 ± 10,000 and 59,000 ± 15,000 (means ± SE) urea molecules/s/channel for UT-A2 and UT-A3, respectively, were obtained. Overall, the UT-A2 and UT-A3 isoforms appear to have identical functional kinetics.
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Wallace, R. John. "Catabolism of Amino Acids by Megasphaera elsdenii LC1." Applied and Environmental Microbiology 51, no. 5 (1986): 1141–43. http://dx.doi.org/10.1128/aem.51.5.1141-1143.1986.
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Neinast, Michael, Danielle Murashige, and Zoltan Arany. "Branched Chain Amino Acids." Annual Review of Physiology 81, no. 1 (February 10, 2019): 139–64. http://dx.doi.org/10.1146/annurev-physiol-020518-114455.
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Branched chain amino acids (BCAAs) are building blocks for all life-forms. We review here the fundamentals of BCAA metabolism in mammalian physiology. Decades of studies have elicited a deep understanding of biochemical reactions involved in BCAA catabolism. In addition, BCAAs and various catabolic products act as signaling molecules, activating programs ranging from protein synthesis to insulin secretion. How these processes are integrated at an organismal level is less clear. Inborn errors of metabolism highlight the importance of organismal regulation of BCAA physiology. More recently, subtle alterations of BCAA metabolism have been suggested to contribute to numerous prevalent diseases, including diabetes, cancer, and heart failure. Understanding the mechanisms underlying altered BCAA metabolism and how they contribute to disease pathophysiology will keep researchers busy for the foreseeable future.
Dissertations / Theses on the topic "Catabolism of mammal amino acids"
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Acworth, I. N. "Studies on the role of changes in the plasma levels of aromatic and branched-chain amino acids." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375218.
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Hou, Chunsheng 1968. "Sulfur amino acid catabolism in a piglet model." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78381.
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A model was developed in growing piglets to study the use of urinary total sulfur excretion as an indicator of sulfur amino acid (SAA) catabolism and the nitrogen (N)/sulfur (S) balance ratio as an indicator of non-protein SAA storage. The recovery of administrated methionine as urinary total S over 48 hours was 106% in well-nourished piglets, but only 69% in protein malnourished piglets. The N/S balance ratio of protein malnourished piglets was lower than that of well-nourished piglets, and this ratio further decreased after methionine administration. We conclude that in a protein malnourished state, relatively more S than N is retained and a significant portion of the S derived from administrated methionine is retained in non-protein pools. These results demonstrate that urinary total S excretion can provide an accurate measure of SAA catabolism; and the N/S balance ratio can provide valuable information about non-protein SAA storage in growing piglets.
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Ganesan, Balasubramanian. "Catabolism of Amino acids to Volatile Fatty Acids by Lactococcus lactis." DigitalCommons@USU, 2005. https://digitalcommons.usu.edu/etd/5509.
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Lactic acid bacteria are essential as flavor producers of cheese and fermented products. They are capable of catabolizing aromatic, branched chain, and sulfur amino acids to flavor compounds. During cheese ripening the numbers of lactococcal colonies decrease, but lactococci survive without replication in culture. This prompted an investigation into possible mechanisms of catabolism of branched chain amino acids into branched chain fatty acids and the physiological relevance of amino acid catabolism to the bacteria. We hypothesized that lactococci catabolize branched chain amino acids to branched chain fatty acids during nonculturability.
Lactococci, lactobacilli, and brevibacteria catabolized both branched chain amino acids and keto acids into branched chain fatty acids. Lactococci survived carbohydrate-limited conditions for over 4 yrs. Their survival was represented by maintaining intracellular ATP, enzyme activity, membrane integrity, capability of ATP- and PMF-dependent substrate transport, transcription, and catabolism of amino acids to fatty acids. Assays conducted with NMR spectroscopy coupled with in silico analysis showed that branched chain substrates are catabolized via keto acids, HMG-CoA, and acetyl-CoA to branched chain fatty acids. A short list of candidate genes was identified for the pathway by gene expression analysis coupled to NMR analysis. The expression of these genes and the presence of the related catabolites were identified in long-term starved cultures of nonculturable lactococci. This verified that catabolism of branched chain amino acids to branched chain fatty acids occurred during the nonculturable state only and in conditions of carbohydrate deprivation. The pathway also facilitated fixation of carbon by lactococci, revealing the mechanism of survival of lactococci over 4 yrs in culture without the addition of external carbon sources. Between strains the availability of carbohydrate and acid stress played significant roles in modulating their ability to produce branched chain catabolites.
The ability of lactococci to catabolize branched chain amino acids during sugar starvation represents a shift in carbon catabolic routes. The identified pathway also represented a balance between catabolism and anabolism, suggesting that the bacteria were in a homeostatic state during nonculturability. We accepted the hypothesis that nonculturable lactococci catabolized branched chain amino acids to branched chain fatty acids during starvation./p>
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Moyes, Christopher D. "Catabolism of osmotically-active amino acids in two groups of osmoconformers, bivalve molluscs and elasmobranchs." Thesis, University of Ottawa (Canada), 1986. http://hdl.handle.net/10393/5139.
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Agnelli, Silvia. "Regulation of amino acid catabolism in rats fed diets with different protein content." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/400005.
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Current lifestyle with high-energy diets and characterized by sedentary is triggering an alarming growth in obesity. Obesity along with metabolic syndrome- related co-morbidities (i.e. insulin resistance, atherosclerosis, sleep apnea, depression, asthma, hypertension and the alteration of blood lipid transport) are the most apparent consequence of the excess energy. Under conditions of excess dietary energy, the body cannot easily dispose of the excess amino-N against the evolutively-adapted schemes that prevent its wastage; thus ammonia and glutamine formation and urea excretion are decreased. High lipid and energy availability limit the utilization of glucose, and high glucose spares the production of ammonium from amino acids, decreasing the synthesis of glutamine and its utilization by the intestine and kidney. In contrast, high protein diets enhance protein synthesis and growth, and the synthesis of non-protein-N-containing compounds. But these outlets are not enough; consequently, less- conventional mechanisms are activated, such as increased synthesis of NO∙ followed by higher nitrite (and nitrate) excretion and changes in the microbiota.
In this study we studied how the initial phase of development of metabolic syndrome can affects the function of liver as main site of amino-N metabolism, and to determine whether doubling the protein content in the diet induced significant changes in enzyme of amino acids metabolism along intestine and on liver.
The common result obtained by these studies is that, both in case of hyperlipidic or hyperproteic diets, elimination of excess N is necessary but cannot be easily carried out through the metabolic pathways/tissues we evaluated, although possible alternative pathways have been taken into consideration.L’estil de vida actual amb les dietes d'alt contingut energètic, i caracteritzat pel sedentarisme, està provocant un creixement alarmant de l'obesitat. L'obesitat, juntament amb les comorbiditats relacionades amb la síndrome metabòlica (és a dir, resistència a la insulina, aterosclerosi, apnea del son, depressió, asma, la hipertensió i l'alteració del transport de lípids en la sang) són la conseqüència més evident de l'excés d’energia. En condicions d'excés d'energia de la dieta, el cos no pot eliminar ràpidament l'excés d'amino-N contra els esquemes adaptats evolutivament i que impedeixin el seu deteriorament; així, la formació d'amoníac i de glutamina i l'excreció d'urea disminueixen. Els elevats nivells de lípids i de la disponibilitat d'energia limiten la utilització de la glucosa, i nivells elevats de glucosa estalvia la producció d'amoni a partir dels aminoàcids, disminuint la síntesi de glutamina i la seva utilització per l'intestí i el ronyó. En contrast, les dietes d’elevat contingut en proteïnes incrementen la síntesi de proteïnes i el creixement, i la síntesi de compostos que contenen N i no són proteïnes. Però aquests mecanismes no són suficients i en conseqüència, s'activen mecanismes menys convencionals, com ara augment de la síntesi de NO ∙ seguides per l’augment del nitrit (i nitrat) i la seva excreció, juntament amb canvis en la microbiota. En aquest treball es va estudiar com la fase inicial de desenvolupament de la síndrome metabòlica pot afectar la funció del fetge com lloc principal del metabolisme d'amino-N, i per determinar si la duplicació del contingut de proteïnes en la dieta induïa canvis significatius en els enzims del metabolisme d'aminoàcids al llarg intestí i al fetge. El resultat genèric obtingut per aquests estudis és que, tant en el cas de que la dieta sigui hiperlipídica o hiperproteica, l'eliminació de l'excés de N és necessària, però no es pot dur a terme fàcilment a través de les vies metabòliques / teixits que avaluem, tot i les possibles vies alternatives s'han tingut en consideració.
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Radkov, Atanas D. "UNVEILING NOVEL ASPECTS OF D-AMINO ACID METABOLISM IN THE MODEL BACTERIUM PSEUDOMONAS PUTIDA KT2440." UKnowledge, 2015. http://uknowledge.uky.edu/pss_etds/67.
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D-amino acids (D-AAs) are the α-carbon enantiomers of L-amino acids (L- AAs), the building blocks of proteins in known organisms. It was largely believed that D-AAs are unnatural and must be toxic to most organisms, as they would compete with the L-counterparts for protein synthesis. Recently, new methods have been developed that allow scientists to chromatographically separate the two AA stereoisomers. Since that time, it has been discovered that D-AAs are vital molecules and they have been detected in many organisms. The work of this dissertation focuses on their place in bacterial metabolism. This specific area was selected due to the abundance of D-AAs in bacteria-rich environments and the knowledge of their part in several processes, such as peptidoglycan synthesis, biofilm disassembly, and sporulation. We focused on the bacterium Pseudomonas putida KT2440 which inhabits the densely populated plant rhizosphere. Due to its versatility and cosmopolitan character, this bacterium has provided an excellent system to study D-AA metabolism.
In the first chapter, we have developed a new approach to identify specific genes encoding enzymes acting on D-AAs, collectively known as amino acid racemases. Using this novel method, we identified three amino acid racemases encoded by the genome of P. putida KT2440. All of the enzymes were subsequently cloned and purified to homogeneity, followed by a complete biochemical characterization. The aim of the second chapter was to understand the specific role of the peculiar broad-spectrum amino acid racemase Alr identified in chapter one. After constructing a markerless deletion of the cognate gene, we conducted a variety of phenotypic assays that led to a model for a novel catabolic pathway that involves D-ornithine as an intermediate. The work in chapter three identifies for the first time numerous rhizosphere-dwelling bacteria capable of catabolizing D-AAs. Overall, the work in this dissertation contributes a novel understanding of D-AA catabolism in bacteria and aims to stimulate future efforts in this research area.
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Weiwei, Dai. "Amino acids regulate hepatic intermediary metabolism-related gene expression via mTORC1-dependent manner in rainbow trout (Oncorhynchus mykiss)." Thesis, Pau, 2015. http://www.theses.fr/2015PAUU3042/document.
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Au cours de ma thèse, nous avons utilisé la truite arc-en-ciel, un poisson carnivore et modèle potentiellement pertinent du diabète, pour étudier des mécanismes de régulation du métabolisme intermédiaire hépatique par les nutriments (acides aminés (AA) et le glucose). Nous nous sommes plus particulièrement intéressés aux voies de signalisation de l’insuline et des acides aminés (Akt et mTORC1). Grâce à l’utilisation de rapamycine, un inhibiteur pharmacologique de mTORC1, nous avons montré que l'activation de mTORC1 stimule l'expression de gènes de la lipogenèse, de la glycolyse et du catabolisme des acides aminés, tandis que la voie de signalisation Akt inhibe celle des gènes impliqués dans la néoglucogenèse. Ces études ont été conduites dans le foie de truite ou en culture primaire d’hépatocytes de truite arc-en-ciel. En outre, nous avons démontré lors de stimulations à court terme in vivo et in vitro que l'expression hépatique des gènes de la lipogenèse est plus sensible à l'apport de protéines alimentaires ou d’AA qu’à l'apport de glucides ou de glucose. De plus, nous avons observé que des taux élevés d’AA conduisent, par le biais de l’activation de la voie de signalisation mTORC1, à une augmentation de l'expression des gènes lipogéniques mais surtout à une répression de l’inhibition de l’expression des gènes de la néoglucogenèse induite par l’insuline. Cet effet s’accompagne d’une augmentation de la phosphorylation de IRS-1 sur le résidu Ser302 qui pourrait être responsable de la baisse de phosphorylation d'Akt et par conséquent d’une inhibition de l’action de l'insuline. Enfin, en réalisant un test de tolérance au glucose chez des truites préalablement traitées avec de la rapamycine, nous avons conclu que la néoglucogenèse hépatique joue un rôle probablement majeur dans le contrôle de l'homéostasie glucidique chez la truite. Ainsi, une absence d’inhibition de la néoglucogenèse pourrait contribuer au maintien de l'hyperglycémie prolongée et au phénotype d’intolérance au glucose caractéristique des poissons carnivores. Cette thèse met en avant le rôle des protéines/AA dans la régulation du métabolisme intermédiaire de la truite et identifie certaines voies de signalisation cellulaire sollicités par les acides aminés pour réguler le métabolisme. Elle permet ainsi d’éclaircir certaines particularités nutritionnelles de la truiteDuring my doctoral study, we used rainbow trout, a representative carnivorous fish and relevant diabetic model, to study the mechanisms underlying the regulation of hepatic intermediary metabolism by nutrients (amino acids (AAs) and glucose), and determine the potential involvement of insulin/Akt and mTORC1 signaling pathways in these regulations. Using acute administration of rapamycin, a pharmacological inhibitor of TOR, we first identified that mTORC1 activation promotes the expression of genes related to fatty acid biosynthesis, glycolysis and amino acid catabolism, while Akt negatively regulates gluconeogenic gene expression in rainbow trout liver and primary hepatocytes. Furthermore, we demonstrated hepatic fatty acid biosynthetic gene expression is more responsive to dietary protein intake/AAs than dietary carbohydrate intake/glucose during acute stimulations in vivo and in vitro. Moreover, we further showed that high levels of AAs up-regulate hepatic fatty acid biosynthetic gene expression through an mTORC1-dependent manner, while excessive AAs attenuate insulin-mediated repression of gluconeogenesis through elevating IRS-1 Ser302 phosphorylation, which in turn impairs Akt phosphorylation and dampens insulin action. Finally, using glucose tolerance test and acute inhibition of rapamycin, we concluded that hepatic gluconeogenesis probably plays a major role in controlling glucose homeostasis, which maybe account for the prolonged hyperglycemia and glucose intolerance phenotype of carnivorous fish. The present thesis brings forward our understandings about the roles of protein/AAs in the regulation of hepatic intermediary metabolism in trout and identifies relevant cellular signaling pathways mediating the action of amino acids on metabolism. It also clarifies some nutritional characteristics of the trout
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Hanselius, Anne, and Karoline Eldemark. "Regulations of catabolic and anabolic mechanisms; the interactions between exercise, carbohydrates and an excessive intake of amino acids : A review of some of the metabolic pathways that affects the homeostasis of the body, as well as β-oxidation and protein synthesis." Thesis, Halmstad University, Halmstad University, Halmstad University, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-4933.
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Insulin as well as glucagon are important hormones in maintaining glucose homeostasis and regulating the metabolism in the body. Insulin receptors (IR) are transmembrane receptors that promote a signal transduction when activated by insulin. This can for example cause an increased influx of glucose into the cell performed by so called glucose transporters (GLUTs). These membrane proteins facilitate the transport of glucose from the blood into the cells, so the cell always has a constant supply of energy. Peroxisome proliferator-activated receptors (PPAR) are nuclear fatty acid receptors. They are activated by lipids and regulate fatty acid transcription. PPARδ/β is located in skeletal muscle and can promote fatty acid catabolism as well as cause a switch in fuel preference from glucose to fatty acids. It has been suggested that ligands for PPARδ could act as insulin sensitizers. The PPARγ coactivator-1α can increase mitochondrial content in skeletal muscle if over expressed. The same is true for endurance exercise.
Hormones released from adipose tissue can cause hyperphagia and obesity if over- or under expressed. They can also work in the opposite way by decreasing appetite with weight loss as an effect. Impaired signalling or dysfunctional receptor can cause insulin resistance, obesity and diabetes. Lipolysis occurs in adipose tissues and is conducted by three enzymes, namely adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL) and monoglyceride lipase (MGL). There are some factors that can increase lipolysis such as caffeine, a low glycemic index, high protein intake and training.
The enzyme PEPCK is involved in the gluconeogensis in the liver and kidney cortex, and also in the glyceroneogenesis in the liver, as well as in brown and white adipose tissue. When overexpressed in skeletal muscle the enzyme increases the muscle activity. The overexpression of the enzyme did promote the β-oxidation as energy source for the muscles during exercise, instead of muscle glycogen as fuel.
The processes of protein synthesis and breakdown are together called protein turnover. Muscle grows when synthesis is greater than breakdown, and withers if breakdown exceeds the level of synthesis. Acute effects of training is catabolic, but long time exercise causes however an increased protein synthesis. Leucine, an essential amino acid, has an important role in the initiation phase of translation. Glutamine is probably important in the regulation of muscle protein synthesis and breakdown. Together with glutamate, aspartate and asparagine, these are responsible for the amino acid metabolism that occurs in the muscles. Protein synthesis reaches its maximum in the recovery phase after intense training.
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Kiyota, Eduardo 1977. "Identificação e caracterização da enzima aminoadípico semialdeído desidrogenase em plantas = Identification and characterization of the aminoadipic semialdehyde dehydrogenase enzyme in plants." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317201.
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Orientador: Paulo ArrudaTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: O amino ácido lisina é catabolizado em plantas e animais pela via da sacaropina. Nesta via, a lisina é convertida a ?-aminoadipato-?-semialdeído (AASA) pela ação da enzima bifuncional lisina-cetoglutarato redutase/sacaropina desidrogenase (LKR/SDH). O intermediário AASA é então convertido a ?-aminoadipato (AAA) pela enzima ?-aminoadipato-?-semialdeído desidrogenase (AASADH). A LKR/SDH já foi bem caracterizada em plantas e animais, mas a atividade enzimática bem como o possível papel fiiológico da AASADH ainda não foi demonstrada em plantas. A via da sacaropina, além do seu importante papel na regulação dos níveis de lisina, está também envolvida em processos de resposta a estresses. Este trabalho está dividido em dois capítulos. No capítulo I descrevemos a identificação do gene que codifica a AASADH em milho e a caracterização da atividade enzimática da enzima em endosperma imaturo de milho. Mostramos que a AASADH é codificada pelo gene Aldh7b1, um gene muito conservado em eucariotos. A enzima codificada pelo gene Aldh7b1 foi parcialmente purificada de endosperma imaturo de milho e através de eletroforese em condições denaturantes e cromatografia em coluna de gel filtração mostramos que a enzima, na sua forma nativa, apresenta-se como um tetrâmero constituído por quatro subunidades de 55 kDa. A AASADH isolada de endosperma imaturo de milho converte o semi-aldeido AASA em AAA. O produto da reação catalisada pela AASADH foi confirmado por cromatografia em camada delgada. No capítulo II discutimos o papel da via sacaropina no desenvolvimento da semente e na resposta de planas jovens de milho a estresses abióticos. As enzimas LKR/SDH e AASADH são co-expressos nas células das camadas da sub-aleurona do endosperma de milho nas fases intermediarias do desenvolvimento. No entanto, embora a proteína AASADH seja produzida no endosperma e no embrião de sementes imaturas e nos tecidos de plantas jovens, a proteína LKR/SDH é detectada unicamente nas células da sub-aleurona das sementes imaturas. A AASADH mostrou atividade máxima a pH 7,4 e Kms para AASA e NAD+ na ordem de micromolar. Em endosperma imaturo a via da sacaropina é induzida por lisina e reprimida por estresse salino, enquanto prolina e ácido pipecólico são significativamente reprimidos por lisina. Em coleóptiles jovens as enzimas LKR/SDH e AASADH são induzidas transcricionalmente por estresses salino, osmótico e oxidativo, mas enquanto que a proteína AASADH acumula nos tecidos sob estresse, a proteína LKR/SDH não é detectada. Nossos resultados indicam que os genes que codificam as enzimas LKR/SDH e AASADH são co-expressos a nível transcricional, mas não a nível traducional. A ausência da proteína LKR/SDH em plantas jovens sob estresses e os altos níveis do seu transcrito serem detectados mostra um desacoplamento transcrição/tradução que podem ter consequências regulatórias ainda desconhecidas
Abstract: Lysine is catabolized in developing plant tissues through the saccharopine pathway. In this pathway, lysine is converted into ?-aminoadipate-?-semialdehyde (AASA) by the bifunctional enzyme lysine-ketoglutarate reductase/saccharopine dehydrogenase (LKR/SDH). AASA is then converted into ?-aminoadipate (AAA) by aminoadipic semialdehyde dehydrogenase (AASADH). LKR/SDH was characterized in higher eukaryotes, but AASADH has not been demonstrated in plants. Furthermore, studies have shown that besides the degradation of lysine, the saccharopine pathway is involved in stress response processes in plants, animals and bacteria. This work was divided into two chapters. Chapter I describes the identification of the gene encoding AASADH and the partial purification and characterization of the enzyme from developing maize endosperm. The enzyme AASADH is encoded by the Aldh7b1 gene, a gene highly conserved among eukaryotes. The enzyme partially purified from developing endosperm and analyzed by SDS-PAGE and gel filtration chromatography behaved, in its native form, as a tetramer constituted by four monomers of 55 kDa. The enzymatic convertion of AASA into AAA was verified by thin layer chromatography. In Chapter II the role of the saccharopine pathway in seed development and stress responses is discussed. LKR/SDH and AASADH are co-expressed in the sub-aleurone cell layers of the developing endosperm; however, although AASADH protein is produced in reproductive and vegetative tissues, the LKR/SDH protein is detectable only in the developing seeds. AASADH showed an optimum pH of 7.4 and Kms for AASA and NAD+ in the micromolar range. In the developing endosperm the saccharopine pathway is induced by exogenous lysine and repressed by salt stress, whereas proline and pipecolic acid synthesis are significantly repressed by lysine. In young coleoptiles the LKR/SDH and AASADH transcriptions are induced by abiotic stress, but while the AASADH protein accumulates in stressed tissues, LKR/SDH does not. Our results indicate that the genes encoding the LKR/SDH and AASADH enzymes are co-expressed at the transcriptional level, but not the translational level. The absence of LKR/SDH protein in young plants under stress despite of the high levels of transcripts being detected suggests a decoupling transcription/translation that may have regulatory consequences yet unknown
Doutorado
Genetica Vegetal e Melhoramento
Doutor em Genetica e Biologia Molecular
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Liang, Yuanxue. "Etude des sources de carbone et d'énergie pour la synthèse des lipides de stockage chez la microalgue verte modèle Chlamydomonas reinhardtii." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0080.
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Les triacylglycérols d'algues (TAG) représentent une source prometteuse de biocarburants. Les principales étapes de la synthèse des acides gras et du métabolisme du TAG des algues ont été déduites de celles des plantes terrestres, mais on en sait peu sur les sources de carbones et d’énergie intervenant dans la synthèse de lipides de réserve. Nous avons donc étudié la synthèse des acides gras chez l’algue modèle Chlamydomonas reinhardtii en utilisant une combinaison d'approches génétiques, biochimiques et microscopiques. Plus précisément, j'ai d'abord examiné la localisation subcellulaire de gouttelettes de lipides dans des cellules d'algues exposées à une forte lumière, conditions où une plus grande quantité de pouvoir réducteur est produite. J'ai ensuite contribué à mettre en évidence que la bêta-oxydation des acides gras est un processus peroxysomal, et que pendant une carence en azote réalisée en conditions photoautotrophe, des mutants dépourvus de la malate déshydrogénase 2 peroxysomale (mdh2) accumulent 50% plus TAG que les souches parentales. Ces résultats nous ont permis de mettre en évidence l'importance du contexte redox cellulaire sur la synthèse lipidique. Cette étude a également permis de révéler l’existence d'un échange d’énergie entre le peroxysome et le chloroplaste. Enfin, en caractérisant des mutants déficients dans la dégradation des acides aminés à chaîne ramifiée (BCAA), j'ai montré que le catabolisme des BCAAs joue un double rôle dans la synthèse de TAG en fournissant des précurseurs carbonés et de l'ATP. L'ensemble de ces travaux ouvert de nouvelles pistes pour l'amélioration génétique future de souches d'algues pour la production de biocarburantsAlgal triacylglycerols (TAG) represent a promising source for biofuel. The major steps for fatty acid synthesis and TAG metabolism have been deduced based on that of land plants, but little is known about carbon and energy sources. To address this question, we investigated fatty acid synthesis in algal cells using a combination of genetic, biochemical and microscopic approaches in the model microalga Chlamydomonas reinhardtii. Specifically, I first examined subcellular localization of lipid droplets in algal cells exposed to high light, a condition favoring production of reducing power. Secondly, I contributed to put on evidence that the beta-oxidation of fatty acids is a peroxisomal process, and that during photoautotrophic nitrogen starvation, knock-out mutants of the peroxisomal malate dehydrogenase 2 (mdh2) made 50% more TAG than parental strains, highlighting the importance of cellular redox context on lipid synthesis. This study also revealed for the first time the occurrence of an energy trafficking pathway from peroxisome to chloroplast. And finally, by characterizing mutants defected in degradation of branched-chain amino acids (BCAAs), I showed that BCAA catabolism plays a dual role in TAG synthesis via providing carbon precursors and ATP. Taken together, this work highlighted the complex interplay between carbon and energy metabolism in green photosynthetic cells, and pointed future directions for genetic improvement of algal strains for biofuel productions
Books on the topic "Catabolism of mammal amino acids"
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B7 (biotin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0011.
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Biotin is a water-soluble B vitamin (vitamin B7) which acts as a coenzyme to carboxylases and has roles in gluconeogenesis, fatty acid synthesis, and amino acid catabolism. Reduced activity of biotin-dependent enzymes (acetyl-CoA carboxylase I and II, and propionyl-CoA carboxylase) alters lipid metabolism and may impair synthesis of polyunsaturated fatty acids and prostaglandins; in addition, biotin has effects on gene expression by binding covalently to histones. Deficiency can be caused by prolonged consumption of egg whites, which contain the biotin-binding protein avidin. Smoking accelerates the degradation of biotin, which can result in marginal biotin deficiency. The effects of deficiency include disruption of immune function and lipid metabolism, with some evidence of teratogenicity in animals. Dietary deficiency is unlikely, although high consumption of egg whites should be avoided in pregnancy.
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Mottram, Linda-Jayne, and Gavin G. Lavery. The metabolic and nutritional response to critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0202.
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The metabolic response to critical illness is complex and affects every body system. The first phase of this response is characterized by increased hypothalamic pituitary activity and resistance (decreased response) to effector hormones in many target tissues. Cytokines released in the early stages of such illness may be important as they appear to stimulate the hypothalamic pituitary axis directly as part of this ‘stress response’. This phase is considered ‘adaptive’ (helpful), increasing the availability of glucose, free fatty acids, and amino acids as substrates for vital organs. However, in prolonged illness, the neuroendocrine response is very different with damped hypothalamic responses, leading to a state in which catabolism predominates, leading to what might be termed the critical illness wasting syndrome. The gastrointestinal (GI) failure often associated with prolonged critical illness appears to be due, at least in part, to an altered neuroendocrine environment. The poor nutritional state associated with GI failure exacerbates the catabolic response, prolonging illness and the period of intensive care management required by the patient. The result is increased mortality and, in survivors, a more prolonged recovery/rehabilitation process.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.
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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.
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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.
Full textAbstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
Book chapters on the topic "Catabolism of mammal amino acids"
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Wu, Guoyao. "Synthesis and Catabolism of Special Substances from Amino Acids." In Amino Acids, 255–332. 2nd ed. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003092742-5.
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Wallin, Reidar, Timothy R. Hall, and Susan M. Hutson. "Regulation of branched chain amino acid catabolism in mammalian tissues: Characterization of the mitochondrial aminotransferase." In Amino Acids, 881–86. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_108.
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Bevington, A., and J. Walls. "Defective Glycolysis and Catabolism of Protein and Amino Acids in Skeletal Muscle during Metabolic Acidosis." In Contributions to Nephrology, 149–55. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000059865.
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"Synthesis and Catabolism of Special Nitrogenous Substances from Amino Acids." In Amino Acids, 168–217. CRC Press, 2013. http://dx.doi.org/10.1201/b14661-9.
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Richard Dickinson, J. "Pathways of Leucine and Valine Catabolism in Yeast." In Branched-Chain Amino Acids, Part B, 80–92. Elsevier, 2000. http://dx.doi.org/10.1016/s0076-6879(00)24221-3.
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Curtin, Á. C., and P. L. H. McSweeney. "Catabolism of Amino Acids in Cheese during Ripening." In Cheese: Chemistry, Physics and Microbiology, 435–54. Elsevier, 2004. http://dx.doi.org/10.1016/s1874-558x(04)80077-0.
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Traut, Thomas W. "β-Alanine Synthase an Enzyme Involved in Catabolism of Uracil and Thymine." In Branched-Chain Amino Acids, Part B, 399–410. Elsevier, 2000. http://dx.doi.org/10.1016/s0076-6879(00)24249-3.
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"Insulin and the regulation of amino acid catabolism and protein turnover." In Metabolic & Therapeutic Aspects of Amino Acids in Clinical Nutrition, 205–20. CRC Press, 2003. http://dx.doi.org/10.1201/9780203010266-23.
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"Cellular metabolism." In Oxford Assess and Progress: Medical Sciences, edited by Jade Chow, John Patterson, Kathy Boursicot, and David Sales. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199605071.003.0014.
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Cellular metabolism is divided into catabolism — responsible for converting nutrients into the energy sources and smaller molecules required for the chemical reactions of the body — and anabolism, which is the interconversion and synthesis of the molecules that maintain the body’s structure and function. This chapter examines the control of metabolism and the central metabolic pathways. Such control includes compartmentalization of metabolic processes and the cooperation between the metabolic activities of different organs. Metabolic control is important because metabolism must match the availability of nutrients to the demand for the products of the metabolic processes and both will vary over time. The synthesis of adenosine triphosphate (ATP), with its high-energy phosphate bond, lies at the heart of these central metabolic pathways. Most of the ATP is produced by oxidative phosphorylation in the mitochondria, but glycolysis and the tricarboxylic acid cycle (also known as the citric acid cycle or Krebs cycle) provide additional amounts. Of the nutrients entering the body from the diet, fat, glucose, and amino acids are the main fuels for cellular metabolism. The utilization of lipids, fatty acids, and ketone bodies is important in metabolism in addition to the key role played by glucose. Glucose is the fuel for energy production in glycolysis. It is also manufactured by gluconeogenesis and stored as glycogen by glycogenesis. It is important to know how different organs utilize different fuels and how energy production alters between the fed state and starvation. Amino-acid metabolism and coenzymes in amino acid oxidation are also important although some details, including the urea cycle, have not been covered here. Energy balance and the relationship between food intake and energy expenditure lead to the concept of body mass index (BMI). The BMI offers a quick method of quantifying the nutritional status of a person, and BMI values may be helpful in assessing the risk of, for example, obesity-related diseases such as type II diabetes and coronary heart disease. Cellular metabolism not only contributes to the medical sciences background to clinical reasoning, but there are also a number of identifiable, inborn errors of metabolism. While individually rare (with incidences of approx. 1–25 per 100,000 births), collectively they present a considerable number of new cases each year.
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Casaer, Michael P., and Greet Van den Berghe. "Nutrition support in acute cardiac care." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 360–72. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0030.
Full textAbstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Full enteral feeding in vasopressor dependent patients recovering from hemodynamic shock increases the risk for bowel ischemia. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
Conference papers on the topic "Catabolism of mammal amino acids"
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Takizawa, Yuko. "Intra-trophic isotopic discrimination of15N/14N associated with the catabolism of amino acids in plants." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.116197.
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