By Massimo Pietropaolo, George S. Eisenbarth (auth.), Boris Draznin MD, PhD, Derek LeRoith MD, PhD (eds.)
In a speedily evolving and intensely vital zone of clinical technology, it is usually tough for the coed, instructor, and researcher to maintain abreast of the entire very important advances. the aim of Molecular Biology ofDiabetes, elements I and II is to carry to those contributors the newest wisdom of diabetes-related learn in a accomplished, but concise demeanour. To this finish, we have now assembled chapters, written by means of lots of the world's specialists within the box, that we think compre hensively survey and synthesize a coherent knowing of the topic. reports of the etiology of style I and sort II diabetes are tremendous fascinating and crucial, on account that we are hoping to 1 day hinder the illness utilizing gene remedy. those elements are coated in Molecular Biology of Diabetes: I. Autoimmunity and Genetics; Insulin Synthesis and Secretion. In sort II diabetes, an abnormality in pancreatic secretion exists concomitantly with peripheral insulin resistance. This abnor mality of insulin secretion is thought to be on the topic of a defect(s) in glucose sensing. Uncoupling of glucose sensing from insulin secre tion could be the the most important step within the pathogenesis of noninsulin-depen dent diabetes. during this quantity, we now have invited authors to explain their stories on all identified elements affecting ~-cell functionality, together with autoimmunity and genetics of diabetes, in addition to molecular mecha nisms of insulin synthesis and secretion. within the previous few years, the main swiftly advancing region of analysis in diabetes has been, actually, regarding insulin action.
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Additional info for Molecular Biology of Diabetes: I. Autoimmunity and Genetics; Insulin Synthesis and Secretion
Table 3 summarizes our current view ofthe pathogenesis oftype I diabetes. The disease develops in the setting of genetic susceptibility determined by alleles both within and outside of the major histocompatibility complex. The disease is the result of progressive plaque-like destruction ofbeta cells within individual islets (insulitis) and overt hypoglycemia develops only after extensive beta cell destruction. During the process of beta cell destruction, a family of autoantigens (present in insulin secretory granules and synaptic-like microvesicles are targeted).
Nature 356: 114, 1992. 56. Calcinaro F, Hao L, Chase HP, Klingensmith G, Lafferty KJ: Detection of cell-mediated immunity in type I diabetes mellitus. J Autoimmun 5:137147,1992. 57. Erlich HA, Griffith RL, Bugawan TL, Ziegler R, Alper C, Eisenbarth GS: Implication ofspecific DQB 1alleles in genetic susceptibility and resistance by identification of IODM siblings with novel HLA-DQB 1 allele and unusual DR2 and DRI haplotypes. Diabetes 40:478-481, 1991. 58. Atkinson MA, Maclaren NK: What causes diabetes?
Any pathogenic scheme at present is only an outline ofthe disease process. In particular, the genes creating diabetes susceptibility outside of the major histocompatibility complex are unknown. It is likely that within this decade, this lack of knowledge will be overcome. Hopefully, safe prevention of the disorder will come with a better understanding of the molecular pathor· ogy of type I diabetes. , Insulin gene polymorphisms, ? , Adjuvant-like exposure) Antigen presentation by B-Iymphocytes and mlocytes to B- and T-cells Class II MHC genes EXpansiorti-islet CD4 T-lymphocytes Islet damage/~-cell secretion Perpetuation/regulation autoimmunity Immunoglobulin gene mutations DR4 haplotypes: high response to insulin and other autoantigens Locallymphokine production Enhanced vascular permeability Enhanced Class I, Class II expression J3-cell toxicity Lymphokines Free radicals CD4/CD8 T-cells NK cells Macrophages ~ Progressive plaque-like J3-cell destruction ~ Type I diabetes 28 Pietropaolo and Eisenbarth References 1.
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