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Books on the topic 'Beta cell insulin secretion'

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Author: Grafiati

Published: 11 March 2023

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1

Susumu, Seino, and Bell Graeme, eds. Pancreatic beta cell in health and disease. [Tokyo]: Springer, 2008.

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2

Kulkarni, Rohit N. Islet cell growth factors. Austin, Tex: Landes Bioscience, 2011.

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3

Liu, Hui-Kang. Modification of the function of insulin-secreting cells by beta-cell toxins, differentiation drugs, insulin mimetics, steriods, and incretin hormones and their stable analogues. [S.l: The Author], 2003.

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4

R, Flatt Peter, and Lenzen Sigurd, eds. Frontiers of insulin secretion and pancreatic B-cell research. London: Smith-Gordon, 1994.

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5

Duffy, Joan. Effects of insulin sensitising agents on pancreatic beta cell function. [S.l: The Author], 2003.

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6

Bonnevie-Nielsen, Vagn. The endocrine pancreas aspects of Ý-cell function in relation to morphology, insulin secretion and insulin content. Oxford: Published for Medisinsk fysiologisk forenings forlag, Oslo by Blackwell Scientific Publications, 1986.

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7

Francesco, Belfiore, ed. Molecular and cell biology of type 2 diabetes and its complications. Basel: Karger, 1998.

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8

patterson, Steven. Homocysteine and the effects of other amino thiols on pancreatic beta cell function and insulin. [S.l: The Author], 2003.

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9

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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10

Seino, Susumu, and Graeme I. Bell. Pancreatic Beta Cell in Health and Disease. Springer, 2009.

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11

Islet Transplantation and Beta Cell Replacement Therapy. Informa Healthcare, 2007.

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12

Shapiro, A. M. James, and James A. M. Shaw. Islet Transplantation and Beta Cell Replacement Therapy. Taylor & Francis Group, 2007.

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13

Shapiro, A. M. James, and James A. M. Shaw. Islet Transplantation and Beta Cell Replacement Therapy. Taylor & Francis Group, 2007.

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14

Kashyap, Sangeeta. Medical Management of Endocrine Disorders after Bariatric Surgery. Edited by Tomasz Rogula, Philip Schauer, and Tammy Fouse. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190608347.003.0015.

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Endocrine complications after bariatric surgery include persistent hyperglycemia in patients with type 2 diabetes who experience initial success with weight loss. This complication occurs in those with a prolonged duration of diabetes (> 8 years) and is related to poor residual pancreatic beta-cell function. Often, weight regain is associated with recurrent diabetes, and strategies that target both weight loss and glycemic control are required. New diabetes agents, such as the SGLT2 inhibitor drug class, offer advantages to diabetes treatment after bariatric surgery. On the other end of the glycemic spectrum, hyperinsulinemic hypoglycemia occurs in patients with and without diabetes prior to surgery and often presents with little or no symptoms (i.e., neuroglycopenia). Treatment strategies involve careful monitoring of blood glucose levels and the use of low-glycemic/high-fiber diets as well as drugs that lower glucose absorption and insulin secretion. Glycemic management after bariatric surgery requires close observation.

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15

(Editor), P. R. Flatt, and S. Lenzen (Editor), eds. Frontiers of Insulin Secretion and Pancreatic B-cell Research. Smith-Gordon & Co Ltd, 1995.

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16

Joseph, Jamie W. beta-cell stimulus-secretion coupling: A role for uncoupling protein 2. 2004.

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17

Yau, Daphne. Insulin resistance precipitates beta-cell dysfunction and beta-cell expansion in a non-obese model of type 2 diabetes. 2005.

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18

(Editor), F. Belfiore, M. Lorenzi (Editor), G. M. Molinatti (Editor), and M. Porta (Editor), eds. Molecular and Cell Biology of Type 2 Diabetes and Its Complications: 5th International Diabetes Conference, Turin, April 10-12, 1997 (Frontiers in Diabetes). S. Karger Publishers (USA), 1998.

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19

Effects of prolonged exercise on the ultrastructure of the pancreatic beta cell and the morphology of the islet of Langerhans. 1985.

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20

Effects of prolonged exercise on the ultrastructure of the pancreatic beta cell and the morphology of the islet of Langerhans. 1985.

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21

Effects of prolonged exercise on the ultrastructure of the pancreatic beta cell and the morphology of the islet of Langerhans. 1985.

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22

Arnoux, Jean-Baptiste, and Pascal de Lonlay. Hyperinsulinemic Hypoglycemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0004.

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Hypoglycemia is a frequent and often overlooked symptom. Indeed, most cases are related to insulin therapy in diabetic patients, to hormone deficiencies, or to very prolonged fasts. In other cases, however, unusual findings (unexplained hypoglycemia, especially if clinically severe, recurrent, postprandial, or in typical relationship to external factors such as food ingestion or exercise, or associated with hepatomegaly) should lead to a careful clinical and biological evaluation. Hyperinsulinemic hypoglycemia is a dysregulation of the glucose-induced insulin secretion. Besides insulinoma and genetic defects of the pancreatic ß-cell (congenital hyperinsulinism, CHI), some other pathophysiological mechanisms can lead to hypoglycemia with biological evidence for an involvement of the insulin signaling pathway (insulin-like substances, autoimmunity, and other).

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23

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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