Livres : « Cataboliti »

1

Suzuki, Koichi, et Judith S. Bond, dir. Intracellular Protein Catabolism. Boston, MA : Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0335-0.

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2

Revhaug, Arthur, dir. Acute Catabolic State. Berlin, Heidelberg : Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-48801-6.

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3

1950-, Revhaug A., dir. Acute catabolic state. Berlin : Springer, 1996.

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4

Rojas, A. E. Carvajal de. Carbon catabolism in streptomyces venezuelae. Manchester : UMIST, 1995.

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5

McVitty, Rosalind Shirley. In vitro studies of folate catabolism. [S.l : The Author], 1997.

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6

Beck, Susan Anne. Catabolic factors in tumour-induced cachexia. Birmingham : Aston University. Department of Pharmaceutical Sciences, 1989.

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7

Floderus, Eugenie. Aminopeptidases and arginine catabolism in oral streptococci. [Stockholm : Karolinska Institute, Dept. of Oral Microbiology], 1990.

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8

Floderus, Eugenie. Aminopeptidases and arginine catabolism in oral straptococci. Stockholm : Kongl. Carolinska Medico Chirurgiska Institutet, 1990.

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9

International Symposium on Intracellular Protein Catabolism (6th 1986 Büchenberg (Magdeburg, Germany)). Intracellular protein catabolism : Abstracts of the 6th symposium. Sous la direction de Aurich H, Kirschke Heidrun, Wiederanders Bernd, Proteolysis Group in Halle et Biochemische Gesellschaft der Deutschen Demokratischen Republik. Halle, Saale : Martin-Luther-Universität Halle-Wittenberg, 1986.

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10

Engel, Norbert G. Chlorophyll catabolism in algae and higher plants : A chemical approach. Freiburg (Schweiz) : Department of Chemistry, Universität Freiburg (Schwiez), 2001.

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11

A, Khairallah Edward, Bond Judith S et Bird John W. C, dir. Intracellular protein catabolism : Proceedings of the Fifth International Symposium on Intracellular Protein Catabolism, held May 29-June 2, 1984, at the Airlie Conference Center, Airlie, Virginia. New York : A.R. Liss, 1985.

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12

Koosha, Homa. Investigations into the expression of catabolic Gene derived from Pseudomonas and Azotobacter. Uxbridge : Brunel University, 1986.

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13

Joshi, Harshad. Investigation of the catabolic plasmid involvement in naphthalene-degrading strains of Pseudomonas spp.. Wolverhampton : University of Wolverhampton, 1995.

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14

Al-Bader, Dhia A. Investigating the role of the oxidative pentose phosphate pathway as the major route of carbohydrate catabolism in the cyanobacterium Synechocystis sp. PCC 6803. [s.l.] : typescript, 1999.

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15

1924-, Suzuki Koichi, Bond Judith S et International Symposium on Intracellular Protein Catabolism (10th : 1994 : Tokyo, Japan), dir. Intracellular protein catabolism. New York : Plenum Press, 1996.

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16

Koichi Suzuki Judith S. Bond. Intracellular Protein Catabolism. Springer US, 2011.

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17

Suzuki, Koichi, et Judith S. Bond. Intracellular Protein Catabolism. Springer London, Limited, 2012.

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18

Revhaug, Arthur. Acute Catabolic State. Springer Berlin / Heidelberg, 2012.

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19

Acute Catabolic State. Springer, 2012.

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20

Revhaug, Arthur. Acute Catabolic State. Springer London, Limited, 2012.

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21

Turk, Vito. Intracellular Protein Catabolism II. Springer London, Limited, 2012.

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22

KHAIRALLAH, EA. Khairallah Intracellular Protein Catabolism. John Wiley & Sons Inc, 1985.

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23

Turk, Vito. Intracellular Protein Catabolism II. Springer, 2012.

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24

Dutz, H., A. Graffi et R. Baumann. 3rd Symposium Intracellular Protein Catabolism. de Gruyter GmbH, Walter, 2022.

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25

Catabolic Diseases ; Nutritional Aspects and Diet Implications. Adhyayan Publishers & Distributors, 2005.

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26

Mottram, Linda-Jayne, et 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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27

Egreteau, Pierre-Yves, et Jean-Michel Boles. Assessing nutritional status in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0204.

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Decreased nutrient intake, increased body requirements, and/or altered nutrient utilization are frequently combined in critically-ill patients. The initial nutritional status and the extent of the disease-related catabolism are the main risk factors for nutrition- related complications. Many complications are related to protein energy malnutrition, which is frequent in the ICU setting. Assessing nutritional status pursues several different goals. Nutritional assessment is required for patients presenting with clinical evidence of malnutrition, with chronic diseases, with acute conditions accompanied by a high catabolic rate, and elderly patients. Recording the patient’s history, nutrient intake, and physical examination, and subjective global assessment allows classification of nutritional status. All the traditional markers of malnutrition, anthropometric measurements and plasma proteins, lose their specificity in the sick adult as each may be affected by a number of non-nutritional factors. Muscle function evaluated by hand-grip strength in cooperative patients and serum albumin provide an objective risk assessment. Several nutritional indices have been validated in specific groups of patients to identify patients at risk of nutritionally-mediated complications and, therefore, the need for nutritional support. A strong suspicion remains the best way of uncovering potentially harmful nutritional deficiencies.

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28

Leyn, P. De. Patterns and Site of Adenosine Triphosphate Catabolism in Lung Tissue. Leuven University Press, 1993.

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29

Perkins, Edward Joseph. The molecular biology of the halogenated aromatic catabolic plasmid pJP4. 1987.

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30

Revhaug, A. Acute Catabolic State (Update in Intensive Care and Emergency Medicine). Springer-Verlag, 1995.

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31

Intracellular protein catabolism : Proceedings of the Fifth International Symposium on Intracellular Protein Catabolism, held May 29-June 2, 1984, at the ... in clinical and biological research). A.R. Liss, 1985.

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32

Casaer, Michael P., et 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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33

Casaer, Michael P., et 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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34

Casaer, Michael P., et 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.

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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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35

The catabolism of glucagon-like peptidea 2 : A novel intestinal growth factor. Ottawa : National Library of Canada, 1998.

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36

Kraus, Jennifer. Nutrient exchange in the Rhizobium-legume symbiosis : Glutamate catabolism by Rhizobium meliloti. 1987.

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37

Blaser, Annika Reintam, et Adam M. Deane. Normal physiology of nutrition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0201.

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Energy is derived from three major categories of macronutrient—carbohydrate, lipid, and protein. While energy requirements to maintain stable weight can be estimated, it is uncertain if meeting these energy requirements improves outcomes in the critically ill. In health, excess energy is stored via non-oxidative metabolism and during periods of inadequate energy delivery catabolism of storage products occurs. Both storing and using the stores cost energy, each may require up to quarter of energy contained in stored nutrient. Excess carbohydrate stored as glycogen is easily available, albeit in a limited amount. Storage of lipid is the largest energy repository, but requires complex metabolism and is limited by low oxidative capacity. Protein catabolism normally contributes less than 5% of energy requirements, but during periods of inadequate energy delivery or increased catabolism there is a marked increase in endogenous protein breakdown.

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38

Sheehan, Patrick J. Starvation effects on the physiology and morphology of catabolic Pseudomonas putida isolates. 1991.

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39

Christianson, Alan. Catabolism Reset Diet : : Repair Your Liver, Stop Storing Fat, and Lose Weight Naturally. Independently Published, 2022.

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40

Guo, Chao. Concentration of genes involved in aromatic catabolism in fuel oil contaminated and noncontaminated soils. 1994.

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41

Metabolism, Structure and Function of Plant Tetrapyrroles : Introduction, Microbial and Eukaryotic Chlorophyll Synthesis and Catabolism. Elsevier, 2019. http://dx.doi.org/10.1016/s0065-2296(19)x0002-6.

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42

Grimm, Bernhard. Metabolism, Structure and Function of Plant Tetrapyrroles : Introduction, Microbial and Eukaryotic Chlorophyll Synthesis and Catabolism. Elsevier Science & Technology Books, 2019.

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43

Krunic, Nancy. Prostaglandin transport and catabolism in the choroid plexus during perinatal and postnatal development in sheep. 1999.

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44

Turner, C. Catabolic Starvation : The Microbiota Diet : The Real Reason You Can't Lose Weight & How to Fix It. Independently Published, 2019.

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45

Energy expenditure and protein catabolism in ventilated trauma patients : The effect of head injury and neuromuscular blockade. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1999.

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46

Rabier, Daniel. Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0083.

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Amino acids present in the different biological fluids belong to two groups: the protein group, with the 21 classical amino acids constituting the backbone of the protein, and the nonprotein group, appearing in different metabolic pathways as intermediate metabolites. It is important to know and to be able to recognize the latter, as they are the markers of many inherited metabolic diseases. Three kinds of pathways must be considered: the catabolic pathways, the synthesis pathways, and the transport pathways. A disorder on a catabolic pathway induces an increase of all metabolites upstream and so an increase of the starting amino acid in all fluids. Any disorder on the synthetic pathway of a particular amino acid will induce a decrease of this amino acid in all fluids. When a transporter is located on a plasma membrane, its deficiency will result in normal or low concentration in plasma concomitant to a high excretion in urine.

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47

Beattie, R. Mark, Anil Dhawan et John W.L. Puntis. Refeeding syndrome. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0011.

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Guidelines for the prevention of refeeding syndrome 82Refeeding syndrome is a term used to describe the various metabolic complications that can arise as a result of instituting nutritional support (enteral or parenteral) in malnourished patients.• Such patients are catabolic and their major sources of energy are fat and muscle; total body stores of nitrogen, phosphate, magnesium, and potassium are depleted....

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48

Tremblay, Mark Stephen. The effects of training status, exercise mode, and exercise duration on endogenous anabolic and catabolic steroid hormones in males. 1994.

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49

Rabier, Daniel. Hyperammonemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0078.

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Ammonia, an end-product of protein and amino acid catabolism toxic to the brain, must be removed quickly from the circulation. Its removal is achieved in two steps: glutamine synthesis and urea synthesis. Hyperammonemia results from either an excess of production or defective elimination. There are two main etiologies of hyperammonemia: inherited or acquired. Inherited causes are mainly related to defective elimination while acquired ones result either from excess production or deficient detoxification. Good laboratory diagnostic tools are necessary to make the right diagnosis.

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50

Raman, Vidya T. Perioperative Management of Diabetes Mellitus Type 1 and 2. Sous la direction de Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi et Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0046.

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Diabetes management offers unique challenges in children and adolescents versus adults especially in the perioperative environment. The obvious challenges of monitoring dietary intake plus possible communication barriers with increased risk of diabetic ketoacidosis and hypoglycemia. Adding the catabolic stressors from surgery also add challenges to the perioperative physician managing the patient’s glycemic control. It is important to work with endocrinology in order to manage their diabetes. Lengthier procedures also complicate glycemic control. It involves sometimes close monitoring of not only glucose but electrolytes and blood and urine ketones.

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