By Massimo Pietropaolo, George S. Eisenbarth (auth.), Boris Draznin MD, PhD, Derek LeRoith MD, PhD (eds.)
In a swiftly evolving and very very important region of scientific technology, it's always tough for the scholar, instructor, and researcher to maintain abreast of all of the very important advances. the aim of Molecular Biology ofDiabetes, elements I and II is to carry to those contributors the most recent wisdom of diabetes-related learn in a complete, but concise demeanour. To this finish, we now have assembled chapters, written by way of lots of the world's specialists within the box, that we think compre hensively survey and synthesize a coherent realizing of the topic. reports of the etiology of kind I and kind II diabetes are tremendous fascinating and crucial, in view that we are hoping to at least one day hinder the ailment utilizing gene treatment. those elements are coated in Molecular Biology of Diabetes: I. Autoimmunity and Genetics; Insulin Synthesis and Secretion. In style II diabetes, an abnormality in pancreatic secretion exists concomitantly with peripheral insulin resistance. This abnor mality of insulin secretion is thought to be relating to a defect(s) in glucose sensing. Uncoupling of glucose sensing from insulin secre tion could be the an important step within the pathogenesis of noninsulin-depen dent diabetes. during this quantity, we've got invited authors to explain their reviews on all recognized components 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, relating to insulin action.
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Extra resources for Molecular Biology of Diabetes: I. Autoimmunity and Genetics; Insulin Synthesis and Secretion
Response of peripheralblood mononuclear cells to glutamate decarboxylase in insulin-dependent diabetes. lAncet 339:458,459, 1992. 55. Latchman D: No diabetes link to hsp65? 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.
A high proportion of T-cells within these lines proliferate to insulin. CD4 T-cell clones, particularly those of Haskins and coworkers, derived from splenocytes that do not respond to insulin, are able to transfer diabetes in nondiabetic mice (52). In humans, Roep and coworkers have reported T-cell responses to a 38 kDa secretory granule protein from rat insulinoma (53), which has not yet been characterized, whereas responses to GAD (54,55), or HSP65 (43) have been described. An extensive characterization of T-cell reactivity to autoantigens related to IDDM, including epitope mapping, is now required.
46. : Peripherin: An islet antigen that is cross-reactive with non-obese diabetic mouse class II gene products. Proc Natl Acad Sci USA 89: 172-176, 1992. 47. Pietropaolo M, Buelow R, Gianani R, Yu L, Eisenbarth GS: Independent assortment of biochemically defined autoantibodies in prediabetic relatives. J Immunoll50:166A (abstract), 1993. Targets of Type I Diabetes 31 48. : Combined analysis of autoantibodies enhances prediction ofIDDM in islet cell antibody (ICA) positive relatives. Autoimmunity (suppl):67 (abstract), 1993.