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Books on the topic 'Glycation'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 May 2024

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Consult the top 33 books for your research on the topic 'Glycation.'

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1

Laurie, Coulston, and Australasian Association of Clinical Biochemists., eds. Diabetes, glycation and complications. Mt. Lawley, W.A: Australasian Association of Clinical Biochemists, 1996.

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2

Colaco, Camilo. The glycation hypothesis of atherosclerosis. New York: Springer, 1997.

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3

The glycation hypothesis of atherosclerosis. New York: Chapman & Hall, 1997.

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4

Abdel-Wahab, Yasserr Hassan Atef. Glycation of insulin: A novel aspect of pancreatic B-cell dysfunction contributing to glucose intolerance. [S.l: The Author], 1993.

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5

Park, Lisa. Advanced glycation endproducts and the development of accelerated atherosclerosis in diabetic apolipoprotein E deficient mice / c Lisa Park. [New Haven, Conn: s.n.], 1997.

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6

Rea, Carol Anne. Glycation and the production of reactive oxygen species: Possible link in the pathogenesis of the vascular complications of diabetes. Birmingham: University of Birmingham, 1991.

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7

Mooney, Mark H. Glucagon-like peptide-1 and gastric inhibitory polypeptide: Effects of N-terminal glycation on hormone degradation, insulin secretion and antihyperglycaemic activity. [S.l: The Author], 2000.

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8

Ansari, Nadeem Ahmad. Closer Look at Glycation. Nova Science Publishers, Incorporated, 2021.

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9

Ansari, Nadeem Ahmad. Closer Look at Glycation. Nova Science Publishers, Incorporated, 2021.

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10

ZOFFOUN, Isaac. Peau: Collagène et Anti-Glycation. Independently Published, 2021.

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11

D'Angelo, A., S. Favaro, and G. Gambaro, eds. Advanced Glycation End Products in Nephrology. S. Karger AG, 2000. http://dx.doi.org/10.1159/isbn.978-3-318-00630-8.

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12

ZOFFOUN, Isaac. Peau: Anti-élastase et Ant-Glycation. Independently Published, 2021.

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13

Bast, Patrik. Advanced Glycation End-Products: Sources and Effects. Nova Science Publishers, Incorporated, 2020.

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14

Bast, Patrik. Advanced Glycation End-Products: Sources and Effects. Nova Science Publishers, Incorporated, 2020.

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15

Cohen, Margo P. Diabetes and Protein Glycation Clinical and Pathophysiologica Relevance. 2nd ed. J B Press Company, 1996.

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16

Ravandi, Amir. Isolation and characterization of low density lipoprotein lipid glycation products. 1999.

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17

Bagchi, Debasis, and Jack N. Losso. Reactive Dicarbonyls, Advanced Glycation End Products and Chronic Degenerative Diseases. CRC Press, 2021.

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18

Chong, Sandra Ann Chen. Diabetes induced glycation of collagen inhibits the binding step of collagen phagocytosis. 2006.

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19

Kamal, Tarek. Significance of Advanced Glycation End-Products (AGE) and the Receptor for AGE (RAGE) in Diabetic Nephropathy. INTECH Open Access Publisher, 2012.

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20

Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski, and Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.

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Advances in our understanding of diabetes in human patients and experimental models indicate that a number of mechanisms may contribute to sensory nerve damage in diabetic polyneuropathy (DPN). In addition to oxidative stress, hyperglycemia and hyperlipidemia, recent research in pain, advanced glycation endproduct (AGE), and proteomics specify a contributory role for altered neuronal calcium homeostasis in DPN. Technology advances indicate neuronal energy balance and mitochondrial biogenesis, fission, and fusion are additional potential mechanisms. The effects of dysregulation or loss of insulin signaling and the effects of glucagon-like peptide-1 (GLP-1) and its receptor (GLP-1R) are also implicated.

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21

Levsky, Oskar. Type 2 Diabetes Defeated by Diet: AGING Has Little to Do with Your AGE but the Glycation of Proteins Such As Hemoglobin A1C. Independently Published, 2019.

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22

The Receptor RAGE in Vascular and Cerebral Dysfunctions. [S.l.]: CAMBRIDGE SCHOLARS PUBLISHING, 2019.

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23

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Diabetic renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0164.

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Diabetic nephropathy is kidney damage occurring as a result of diabetes mellitus. Overt diabetic nephropathy is defined as proteinuria greater than 0.5 g/day. Diabetic nephropathy has a complicated pathogenesis including glomerular hypertension with hyperfiltration and advanced glycation end products. Poor glycaemic control is associated with progression to microalbuminuria and overt diabetic nephropathy. The lifetime risk is fairly equivalent for type 1 and type 2 diabetes mellitus. Early disease is usually asymptomatic. Hyperglycaemia causes an osmotic diuresis and, thus, diabetes can present with polyuria. Hypertension develops with microalbuminuria; oedema indicates abnormal sodium and water retention and, occasionally, the development of nephrotic syndrome. Patients with diabetes, perhaps due to accompanying cardiac disease, are particularly susceptible to fluid overload and uraemic symptoms. End-stage renal disease can occur as early as when the estimated glomerular filtration rate is 15 ml/min 1.73 m−2.

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24

(Editor), Angela D'Angelo, Silvana Favaro (Editor), and Giovanni Gambaro (Editor), eds. Advanced Glycation End Products in Nephrology: Meeting on Advanced Glycosylation End-Products in Nephrology: Much More Than Diabetic Nephropathy, Padua, ... Padua, Italy (Contributions to Nephrology). S. Karger Publishers (USA), 2000.

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25

Dietary AGEs and Their Role in Health and Disease. Taylor & Francis Group, 2017.

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26

Uribarri, Jaime. Dietary AGEs and Their Role in Health and Disease. Taylor & Francis Group, 2017.

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27

Uribarri, Jaime. Dietary AGEs and Their Role in Health and Disease. Taylor & Francis Group, 2017.

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28

Uribarri, Jaime. Dietary AGEs and Their Role in Health and Disease. Taylor & Francis Group, 2017.

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29

Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.

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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM₂) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM₂ are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM₂ and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM₂, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM₂ in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.

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30

Zapico, Sara C. Mechanisms Linking Aging, Diseases and Biological Age Estimation. Taylor & Francis Group, 2017.

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31

Zapico, Sara C. Mechanisms Linking Aging, Diseases and Biological Age Estimation. Taylor & Francis Group, 2017.

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32

Zapico, Sara C. Mechanisms Linking Aging Diseases and Biological Age Estimation. Taylor & Francis Group, 2021.

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33

Mechanisms Linking Aging, Diseases and Biological Age Estimation. Taylor & Francis Group, 2016.

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