The present volume summarizes current research on type 2 diabetes, its etiology, pathogenesis and long-term vascular and neurological consequences, with special emphasis on molecular and biochemical mechanisms. Alterations in insulin secretion are comprehensively treated, focusing on the role of glucokinase as glucose sensor. Moreover, insulin action is analyzed with regard to both nonoxidative glucose utilization and glucose oxidation. Concerning the complications in chronic diabetes, topics covered include the effects of high glucose concentration on cellular and endothelial functions and on the glucose phosphorylation rate in non-insulin-sensitive tissues. Furthermore, the role of oxidative stress and advanced glycation end products as well as the significance of alterations in lipoprotein structure are considered. Finally, the pericyte loss in retinopathy and microalbuminuria as related to cardiovascular risk are discussed. Taken as a whole, the contributions included in this book represent a large body of information that will be of great interest to diabetologists, endocrinologists and internists interested in both the basic and clinical aspects of diabetes and its complications.
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ISBN-13
978-3-8055-6644-5 (9783805566445)
Schweitzer Klassifikation
Part 1 Insulin secretion: insulin secretion in type II diabetes; the distinction between "glucose setpoint", "glucose threshold" and "glucose sensor" is critical for understanding the role of the pancreatic beta-cell in glucose homeostasis. Part II Insulin action: the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase system; metabolic aspects of glycogen synthase activation; regulation of glucose oxidation and pyruvate dehydrogenase activity in human skeletal muscle; similar apolipoprotein E phenotype distribution in "high triglyceride responders" and type 2 diabetic patients; effect of intensive glycemic control on fibrinogen plasma levels in diabetic subjects; high glucose increases monolayer permeability to macromolecules in retinal endothelial cells; vascular endothelial growth factor production by human mesangial cells; alterations of retinal microvascular cell glycoproteins by advanced glycation end products; skin microangiopathy - the macroangiopathy is responsible for local differences in type II diabetes; dehydroepiandrosterone prevents the decrease in bovine retinal capillary pericytes number induced in vitro by high glucose; stimulation by aldohexoses of D-fructose phosphorylation by human B-cell glucokinase; oxidative damage induced by acute hyperglycemia is reduced by dehydroepiandrosterone supplementation in the rat.
