Titlebook: Comparison of Type I and Type II Diabetes; Similarities and Dis Mladen Vranic,Charles H. Hollenberg,George Steiner Book 1985 The Editor(s)

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The Genealogy of Brownian Excursions,it, Baumann and colleagues compared the same normal women, pre-and postpartum, to assess these relationships. (Fig. 1). They demonstrated that insulin binding to monocytes and red blood cells at the time of the insulin resistance of late pregnancy is the same or slightly greater than during the lute

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https://doi.org/10.1007/978-3-642-57552-5 absence of obesity may mark heterogeneous groups of Type II diabetic patients, in addition to the importance of obesity in uncovering an insulin secretory defect by causing insulin resistance. There is heterogeneity in susceptibility to vascular disease within NIDDM and MODY. The natural history of

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Uwe Mien,Alexandros Tassinopoulosnent is involved in NIDDM evidenced by a high concordance in monozygotic twins. Nevertheless, there is much evidence of genetic heterogeneity. At the present time no clear cut genetic marker has been defined. The human insulin gene has been cloned and by Southern blot hybridization analysis of perip

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https://doi.org/10.1007/978-3-642-57552-5atients have a retarded form of IDDM. It is possible that the combination of specific Class II antigen molecule(s) and an invading antigen (virus, bacterium, chemical etc.) presented to the immune system triggers the formation of effector cells such as B lymphocytes and cytotoxic T lymphocytes which

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Hans-Peter Gatzweiler,Wilfried Görmarucose uptake characterizes patients with NIDDM, but that it could also exist in patients with IDDM. However, in the latter instance the resistance appeared to be related to degree of metabolic control, and it seemed to us that insulin sensitivity was normal in patients with IDDM well-controlled on i

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Constanze Vorwerg,Gert Rickheitrly, insulin responses to nonglucose stimuli such as arginine often appear normal in NIDDM because of potentiation by hyperglycemia. However, insulin responses to arginine are lower than those of nondiabetic controls when compared at multiple matched glucose levels. Indeed, maximal potentiation by g

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