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Livros sobre o tema "Energy and glucose homeostasis"

Autor: Grafiati
Publicado: 28 de setembro de 2024

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1

Mladen, Vranic, Efendić Suad e Hollenberg Charles H. 1930-, eds. Fuel homeostasis and the nervous system. New York: Plenum Press, 1991.

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2

institutet, Karolinska, ed. Food deprivation and glucose homeostasis in hemorrhagic stress. Stockholm: [s.n.], 1987.

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3

1950-, Pagliassotti Michael J., Davis Stephen N. 1955- e Cherrington Alan 1946-, eds. The role of the liver in maintaining glucose homeostasis. Austin: Landes, 1994.

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4

Polakof, Sergio. Brain glucosensing: Physiological implications. Hauppauge, N.Y: Nova Science Publishers, 2010.

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5

Sarabia, Vivian E. Calcium homeostasis and regulation of glucose uptake in human skeletal muscle cells in culture. Ottawa: National Library of Canada, 1990.

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6

Hodakoski, Cindy Marie. P-REX2 PH Domain Inhibition of PTEN Regulates Transformation, Insulin Signaling, and Glucose Homeostasis. [New York, N.Y.?]: [publisher not identified], 2012.

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7

Miller, Janette Brand. The new glucose revolution pocket guide to sugar & energy. New York: Marlowe, 2004.

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8

Gema, Frühbeck, e Nutrition Society (Great Britain), eds. Peptides in energy balance and obesity. Wallingford, Oxfordshire: CABI Pub. in association with the Nutrition Society, 2009.

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9

Muromt͡sev, V. A. Medit͡sina v XXI veke: Ot drevneĭshikh tradit͡siĭ do vysokikh tekhnologiĭ. Sankt-Peterburg: Izd-vo "Intan", 1998.

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10

Pool, Ontario Assessment Instrument, ed. Energy and the living cell: Draft. Toronto: Minister of Education, Ontario, 1989.

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11

Ross Conference on Medical Research (14th 1994 Carefree, Ariz.). Type II diabetes: Glucose homeostasis, complications, and novel therapies : report of the Fourteenth Ross Conference on Medical Research. Columbus, Ohio: Ross Products Division, Abbott Laboratories, 1995.

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12

1931-, Nakagawa Hachirō, ed. Central regulation of energy metabolism with special reference to circadian rhythm. Boca Raton, Fla: CRC Press, 1992.

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13

Hall, Jessica Ann. Thyroid Hormone and Insulin Metabolic Actions on Energy and Glucose Homeostasis. 2014.

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14

(Editor), Mladen Vranic, Suad Efendic (Editor) e Charles H. Hollenberg (Editor), eds. Fuel Homeostasis and the Nervous System (Advances in Experimental Medicine and Biology). Springer, 1991.

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15

Szablewski, Leszek, ed. Glucose Homeostasis. InTech, 2014. http://dx.doi.org/10.5772/57190.

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16

Szablewski, Leszek, ed. Glucose Homeostasis and Insulin Resistance. BENTHAM SCIENCE PUBLISHERS, 2012. http://dx.doi.org/10.2174/97816080518921110101.

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17

Carneiro, Lionel, Virginie Aubert e Claude Knauf, eds. Neural Control of Energy Homeostasis and Energy Homeostasis Regulation of Brain Function. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-003-9.

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18

Carneiro, Lionel, Virginie Aubert e Claude Knauf, eds. Neural Control of Energy Homeostasis and Energy Homeostasis Regulation of Brain Function. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-003-9.

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19

Biology: Communication, Homeostasis and Energy. Hodder Education Group, 2009.

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20

Biology: Energy, Homeostasis and the Environment. Hodder Education Group, 2016.

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21

Biology A: Communication, Homeostasis and Energy. Hodder Education Group, 2016.

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22

Tao, Ya-Xiong. Glucose Homeostatis and the Pathogenesis of Diabetes Mellitus. Elsevier Science & Technology Books, 2013.

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23

Baggio, Laurie L. The role of incretin hormones in glucose homeostasis. 2001.

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24

Michel, Maximilian, ed. Comparative Studies of Energy Homeostasis in Vertebrates. Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-560-7.

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25

Fosbery, Richard. Biology, Unit F214: Communication, Homeostasis and Energy. Hodder Education Group, 2010.

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26

Pardee, Joel D., e Suresh Tate. Metabolism of Carbohydrates: Glucose Homeostasis in Fasting and Diabetes. Morgan & Claypool Life Science Publishers, 2012.

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27

Otto-Buczkowska, E. Alterations in Glucose Homeostasis in Children, Adolescents and Young Adults: What's New? Nova Science Publishers, Incorporated, 2015.

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28

Fosbery, Richard. OCR A2 Biology Unit F214: Communication Homeostasis and Energy. Hodder Education Group, 2009.

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29

Zilberter, Yuri, ed. The link between brain energy homeostasis and neuronal activity. Frontiers Media SA, 2013. http://dx.doi.org/10.3389/978-2-88919-127-7.

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30

Fosbery, Richard. Ocr A2 Biology Unit F214: Communication, Homeostasis and Energy. Hodder Education Group, 2009.

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31

Fosbery, Richard. OCR A2 Biology Unit F214: Communication, Homeostasis and Energy. Hodder Education Group, 2009.

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32

Tao, Ya-Xiong. G Protein-Coupled Receptors in Energy Homeostasis and Obesity Pathogenesis. Elsevier Science & Technology Books, 2013.

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33

Tao, Ya-Xiong. G Protein-Coupled Receptors in Energy Homeostasis and Obesity Pathogenesis. Elsevier Science & Technology Books, 2013.

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34

G Protein-Coupled Receptors in Energy Homeostasis and Obesity Pathogenesis. Elsevier, 2013. http://dx.doi.org/10.1016/c2010-0-68600-7.

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35

Murer, Heini, Jürg Biber e Carsten A. Wagner. Phosphate homeostasis. Editado por Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0025.

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Inorganic phosphate ions (H2PO4−/ HPO42−) (abbreviated as Pi) are involved in formation of bone and generation of high-energy bonds (e.g. ATP), metabolic pathways, and regulation of cellular functions. In addition, Pi is a component of biological membranes and nucleic acids. Only about 1% of total body Pi content is present in extracellular fluids, at a plasma concentration in adults within the range 0.8–1.4 mMol/L (at pH 7.4 mostly as HPO42−), with diurnal variations of approximately 0.2 mM. A small amount of plasma Pi is bound to proteins or forms complexes with calcium. Under normal, balanced conditions, absorption of dietary Pi along the small intestine equals the output of Pi via kidney and faeces. Renal excretion of Pi represents the key determinant for the adjustment of normal Pi plasma concentrations. Renal reabsorption of Pi occurs along the proximal tubules by sodium-dependent Pi cotransporters that are strictly localized at the apical brush border membrane. Parathyroid hormone (PTH) and FGF23 are key regulators amongst a myriad of factors controlling excretion of Pi in urine, mostly by changes of the apical abundance of Na/Pi cotransporters. Hypophosphataemia may result in osteomalacia, rickets, muscle weakness, and haemolysis. Hyperphosphataemia can lead to hyperparathyroidism and severe calcifications in different tissues.
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36

Houillier, Pascal. Magnesium homeostasis. Editado por Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.

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Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and net entry of magnesium into extracellular fluid. In the kidney, magnesium is reabsorbed in the proximal tubule, the thick ascending limb of the loop of Henle (TALH), and the distal convoluted tubule (DCT). Magnesium absorption is mainly paracellular in the proximal tubule and TALH, whereas it is transcellular in the DCT. The hormone(s) regulating renal magnesium transport and blood magnesium concentration are not fully understood. Renal tubular magnesium transport is altered by a number of hormones, mainly in the TALH and DCT. Parathyroid hormone, calcitonin, arginine vasopressin, ß-adrenergic agonists, and epidermal growth factor, all increase renal tubular magnesium reabsorption; in contrast, prostaglandin E2 decreases magnesium reabsorption. Non-hormonal factors also influence magnesium reabsorption: it is decreased by high blood concentrations of calcium and magnesium, probably via the action of divalent cations on the calcium-sensing receptor; metabolic acidosis decreases, and metabolic alkalosis increases, renal magnesium reabsorption.
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37

Unniappan, Suraj, Ian Orchard e María Jesús Delgado, eds. Neuroendocrine Control of Energy Homeostasis in Non-mammalian Vertebrates and Invertebrates. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-912-0.

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38

Rohas, Lindsay Merritt. A fundamental system of cellular energy homeostasis regulated by PGC-1alpha. 2007.

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39

Biology: Science of Life, Cell Theory, Evolution, Genetics, Homeostasis and Energy. CreateSpace Independent Publishing Platform, 2016.

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40

OCR A2 Biology Student Unit Guide: Unit F214 Communication, Homeostasis and Energy. Hodder Education Group, 2012.

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41

Fosbery, Richard. Ocr A2 Biology Student Unit Guide: Unit F214 Communication Homeostasis and Energy. Hodder Education Group, 2012.

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42

Walls, Anne B., Lasse K. Bak, Arne Schousboe e Helle S. Waagepetersen. Astroglia and Brain Metabolism: Focus on Energy and Neurotransmitter Amino Acid Homeostasis. Morgan & Claypool Life Science Publishers, 2015.

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43

Walls, Anne B., Lasse K. Bak, Arne Schousboe e Helle S. Waagepetersen. Astroglia and Brain Metabolism: Focus on Energy and Neurotransmitter Amino Acid Homeostasis. Morgan & Claypool Publishers, 2015.

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44

Fosbery, Richard. OCR A2 Biology Student Unit Guide - Unit F214: Communication, Homeostasis and Energy. Hodder Education Group, 2012.

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45

Fosbery, Richard. OCR A2 Biology Student Unit Guide: Unit F214 Communication, Homeostasis and Energy. Hodder Education Group, 2012.

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46

Wolever, Thomas M. S., Kaye Foster-Powell e Jennie Brand-Miller. The Glucose Revolution Pocket Guide to Sugar and Energy. Avalon Publishing Group, 2000.

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47

Burton, Derek, e Margaret Burton. Metabolism, homeostasis and growth. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198785552.003.0007.

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Metabolism consists of the sum of anabolism (construction) and catabolism (destruction) with the release of energy, and achieving a fairly constant internal environment (homeostasis). The aquatic external environment favours differences from mammalian pathways of excretion and requires osmoregulatory adjustments for fresh water and seawater though some taxa, notably marine elasmobranchs, avoid osmoregulatory problems by retaining osmotically active substances such as urea, and molecules protecting tissues from urea damage. Ion regulation may occur through chloride cells of the gills. Most fish are not temperature regulators but a few are regional heterotherms, conserving heat internally. The liver has many roles in metabolism, including in some fish the synthesis of antifreeze seasonally. Maturing females synthesize yolk proteins in the liver. Energy storage may include the liver and, surprisingly, white muscle. Fish growth can be indeterminate and highly variable, with very short (annual) life cycles or extremely long cycles with late and/or intermittent reproduction.
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48

Glucose Revolution: Exercise Lowers Insulin Resistance and Improves the Body's Ability to Convert Glucose into Energy. Independently Published, 2022.

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49

Bender, David A. 2. Energy nutrition. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199681921.003.0002.

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Apart from water, the body’s first requirement under all conditions is for an energy source to perform physical and chemical work. ‘Energy nutrition’ explains that the metabolic fuels to provide this energy are derived from fats, carbohydrates, protein, and alcohol in the diet. The constituents of a meal provide these fuels directly for a few hours. Simultaneously, reserves of fat and carbohydrate are laid down for use during fasting between meals. Only about one-third of the average person’s energy expenditure is for voluntary activity; two-thirds is required for maintenance of the body’s functions, metabolic integrity, and homeostasis of the internal environment. Energy expenditure, energy balance, and physical activity are all discussed.
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50

Imaging of Energy Metabolites (Atp, Glucose and Lactate) in Tissue Sections: A Bioluminescent Technique. Lubrecht & Cramer, Limited, 1990.

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