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Books on the topic 'Insulin role in lactation'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

Mahood, I. Kim. Glycated insulin and its role in the pathogenesis of diabetics. [S.l: The Author], 2003.

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2

Khan, Frances Rosemary. The role of insulin and the insulin-like growth factors in the proliferation of the rat thymic lymphocyte. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

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3

Willetts, Alison. The role of cytoskeletal proteins in the mechanism of insulin release. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1988.

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4

Farese, Robert V. The role of protein kinase C in insulin action, resistence and secretion. Austin: R.G. Landes, 1994.

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5

Playford, Martin P. The role of the type 1 insulin-like growth factor receptor in cancer biology. Oxford: Oxford Brookes University, 2000.

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6

Cho, Charles Young. Role of oxidative stress in two models of insulin resistance within primary rat adipocytes. Ottawa: National Library of Canada, 1999.

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7

Belbrahem, Atika. Characterisation of protein Kinase C in chick embryo tissues and hepatocytes: Role in insulin signalling. Manchester: University of Manchester, 1994.

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8

Smulker, Simon R. Determination and characterization of the functional role nitric oxide in the regulation of insulin release. Ottawa: National Library of Canada, 2002.

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9

Miller, Stella-Maria. The expression and putative role of the insulin-like growth factor genes in human ovary. Manchester: University of Manchester, 1996.

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10

Dahl, Douglas Middleton. The hormonal and humoral regulators of myocardial protein metabolism: The in vivo measurement of the physiologic role of insulin and amino acids in cardiac protein kinetics. [s.l: s.n.], 1992.

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11

Das, Undurti N. Metabolic syndrome pathophysiology: The role of essential fatty acids. Ames, Iowa: Wiley-Blackwell, 2010.

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12

Lawlor, Margaret Ann. The role of the insulin-like growth factor-II/mannose-6-phosphate receptor in embryonic development. Dublin: University College Dublin, 1998.

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13

Macfarlane, Wendy Margaret. An investigation of the role of the [beta] cell transcription factor IUF1 in the glucose sensitivity of insulin gene transcription, and in islet cell ontogeny. Birmingham: University of Birmingham, 1995.

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14

Association, American Diabetes, ed. American Diabetes Association guide to medical nutrition therapy for diabetes. 2nd ed. Alexandria, Va: American Diabetes Association, 2012.

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15

Cruz, Lisa M. Reyes, and Douglas C. Ortiz Gutierrez. Lactation: Natural Processes, Physiological Responses and Role in Maternity. Nova Science Publishers, Incorporated, 2013.

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16

Mielke, John Gordon. A physiopathological role for insulin within the brain. 2004.

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17

Prunty, Danielle M. The role of leu-enkephalin in the suckling induced prolactin secretory response in lactating female rats: Immunoneutralization and DOPA accumulation studies. 1995.

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18

Prunty, Danielle M. The role of leu-enkephalin in the suckling induced prolactin secretory response in lactating female rats: Immunoneutralization and DOPA accumulation studies. 1995.

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19

Harry, Keen, ed. CSII in diabetes: An evaluation ofthe role of continuous subcutaneous insulin infusion in diabetes. Guildford: Update-Siebert, 1987.

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20

Klosterman, Shannon Colleen. The role of dynorphin in the suckling induced prolactin response in postpartum lactating female rats. 1995.

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21

K, Raizada Mohan, and LeRoith Derek 1945-, eds. The Role of insulin-like growth factors in the nervous system. New York, N.Y: New York Academy of Sciences, 1993.

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22

Roper, Michael Gabriel. Role of insulin signaling in pancreatic beta cells and measurement of insulin release from islets of langerhans using a microfluidic chip. 2003.

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23

Konrad, Daniel. The role of GLUT4 activation in glucose uptake: Potential implication for insulin resistance? 2003.

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24

Das, Undurti N. Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids. Wiley & Sons, Incorporated, John, 2009.

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25

(Editor), Elena Sebokova, Barbara V. Howard (Editor), and Eric Ravussin (Editor), eds. Lipids and Insulin Resistance: The Role of Fatty Acid Metabolism and Fuel Partitioning (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2002.

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26

Colon cancer promotion, insulin resistance and metabolic measures: The role of dietary calcium, vitamin D and fat. Ottawa: National Library of Canada, 2000.

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27

Agiostratitis, Efstratios. Investigation of the role of plasma non-esterified fatty acid (NEFA) levels in circadian rhythmicity of insulin sensitivity. 1996.

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28

(Editor), Iwar Klimes, Elena Sebokova (Editor), Barbara V. Howard (Editor), and Eric Ravussin (Editor), eds. Lipids and Insulin Resistance: The Role of Fatty Acid Metabolism and Fuel Partitioning (Annals of the New York Academy of Sciences, V. 967). New York Academy of Sciences, 2002.

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29

Basciano, Heather. Development and characterization of a novel animal model of diet-induced insulin resistant diabetes and metabolic dyslipidemia: Mechanistic interactions between dietary fructose, fat and cholesterol, and the possible role of liver X receptor in the induction of metabolic syndrome. 2006.

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30

D, Matthews Dawn, ed. Diabetes sourcebook: Basic consumer health information about Type 1 diabetes (insulin-dependent or juvenile-onset diabetes), Type 2 diabetes (noninsulin-dependent or adult-onset diabetes, gestational diabetes, impaired glucose tolerance (IGT), and related complications, such as amputation, eye disease, gum disease, nerve damage, and end-stage renal disease : including facts about insulin, oral diabetes medications, blood sugar testing, and the role of exercise and nutrition in the control of diabetes : along with a glossary and resources for further help and information. 3rd ed. Detroit, Mich: Omnigraphics, 2003.

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31

Madl, Ulrike. Pathophysiology of glucose control. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0258.

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Hyperglycaemia is a frequent phenomenon in critically-ill patients, associated with increased morbidity and mortality. Hyperglycaemia results in cellular glucose overload and toxic adverse effects of glycolysis and oxidative phosphorylation, especially in tissues with insulin-independent glucose uptake, and acute hyperglycaemia can exert a variety of negative effects. It is the main side effect of intensive insulin therapy. Both severe and moderate hypoglycaemia are independent risk factors of mortality in critically-ill patients. Prolonged hypoglycaemia induces neuronal damage, but may also have adverse cardiovascular effects. Several risk factors predispose critically-ill patients to hypoglycaemic events. Rapid glucose fluctuations may induce oxidative stress and lead to vascular damage. Glucose complexity is a marker of endogenous glucose regulation. Association between hyperglycaemia and outcome is weaker in diabetic critically-ill patients than in non-diabetic patients. Pre-admission glucose control in diabetic critically-ill patients plays a role in the response to glucose control and mortality.

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32

Lameire, Norbert. Prevention of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0226_update_001.

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This chapter summarizes the pharmacological interventions that can be used in the prevention of acute kidney injury (AKI). These following interventions are discussed: the use and selection of vasopressors; the administration of loop diuretics and mannitol; vasodilating drugs including dopamine, atrial natriuretic peptide, nesiritide, fenoldopam, and adenosine antagonists. The role of N-acetylcysteine in the prevention of contrast-induced AKI and cardiac surgery is discussed. The chapter concludes with a summary of the potential role of insulin-like growth factor and erythropoietin in the prevention of AKI.

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33

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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34

Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.

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35

Segal, David. One Hundred Patents That Shaped the Modern World. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198834311.001.0001.

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The Internet has allowed people to access information that previously was difficult to obtain. It is important to know the information is true and accurate and does not represent ‘fake news’ or alternative facts. Patents describe inventions and contain accurate information, as patents are examined and their accuracy can be challenged. This book shows how patents and the inventions they describe have shaped the modern world, that is the world in the twenty-first century. Patent documents that date from the mid-nineteenth century to the present time are used in the text and the subject matter covers many technical areas: for example, Morse code, the diode, triode, transistors, television, frozen foods, ring-pulls for soft drink cans, board games such as Monopoly, gene editing, metamaterials, MRI, computerised tomography, insulin and monoclonal antibodies such as Herceptin. Up to a page of text is used for each entry and the text is backed up by drawings from patent documents. Patent numbers are included to allow interested readers to trace the documents. Inventions described in the patents are placed in a historical perspective. For example, the role of the cavity magnetron and radar are described in the context of the Second World War, whereas the diode is discussed in the development of broadcasting at the beginning of the twentieth century. Entries cover examples from life sciences, engineering and physical sciences in the modern world.

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36

J, Franz Marion, Bantle John P. 1947-, and American Diabetes Association, eds. American Diabetes Association guide to medical nutrition therapy for diabetes. Alexandria, Va: American Diabetes Association, 1999.

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37

Association, American Diabetes. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes (Clinical Education Series). American Diabetes Association, 2003.

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