Diabetes Pathogenesis (diabetes + pathogenesis)

Distribution by Scientific Domains


Selected Abstracts


Coxsackievirus B4 and type 1 diabetes pathogenesis: contribution of animal models

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 7 2009
H. Jaïdane
Abstract The role of enteroviruses, in particular type B coxsackieviruses (CV-B), in type 1 diabetes (T1D) pathogenesis is supported by epidemiological, clinical and experimental observations. The investigation of T1D pathogenesis benefits from the contribution of animal models called spontaneously diabetic. Among these animals the non-obese diabetic (NOD) mouse and the bio-breeding diabetes-prone (BBDP) rat present a genetic susceptibility manifested by the expression of an autoimmune diabetes similar to the pathology observed in human beings. Other models whose genetic predisposition is less known are of considerable contribution as well. Numerous major observations relative to several aspects of T1D pathogenesis in the context of CV-B infections, such as susceptibility, diabetogenicity, pancreatotropism, mechanisms of , cells destruction and others, have been deduced thanks to investigations with animal models. Despite their limits, these models are necessary in improving our knowledge of the role of enteroviruses, like CV-B4, in the pathogenesis of T1D, and the recent advances ensuing from their contribution may have important therapeutic and preventive spin-offs. Copyright © 2009 John Wiley & Sons, Ltd. [source]


SUMO4 and its role in type 1 diabetes pathogenesis

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2008
Cong-Yi Wang
Abstract Susceptibility to type 1 diabetes (T1D) is determined by interactions of multiple genes with unknown environmental factors. Despite the characterization of over 20 susceptibility regions for T1D, identification of specific genes in these regions is still a formidable challenge. In 2004, we first reported the cloning of a novel, small ubiquitin-like modifier (SUMO) gene, SUMO4, in the IDDM5 interval on chromosome 6q25, and presented strong genetic and functional evidence suggesting that SUMO4 is a T1D susceptibility gene. Subsequent studies have consistently confirmed this association in multiple Asian populations despite controversial observations in Caucasians. In this review, we will update the genetic evidence supporting SUMO4 as a T1D susceptibility gene and discuss the possible explanations for the discrepant associations observed in Caucasians. We will then discuss the mechanisms through which SUMO4 contributes to the pathogenesis of T1D. Copyright © 2007 John Wiley & Sons, Ltd. [source]


Role of histone and transcription factor acetylation in diabetes pathogenesis

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 5 2005
Steven G. Gray
Abstract Globally, diabetes (and, in particular, type 2 diabetes) represents a major challenge to world health. Currently in the United States, the costs of treating diabetes and its associated complications exceed $100 billion annually, and this figure is expected to soar in the near future. Despite decades of intense research efforts, the genetic basis of the events involved in the pathogenesis of diabetes is still poorly understood. Diabetes is a complex multigenic syndrome primarily due to beta-cell dysfunction associated with a variable degree of insulin resistance. Recent advances have led to exciting new developments with regard to our understanding of the mechanisms that regulate insulin transcription. These include data that implicate chromatin as a critical regulator of this event. The ,Histone Code' is a widely accepted hypothesis, whereby sequential modifications to the histones in chromatin lead to regulated transcription of genes. One of the modifications used in the histone code is acetylation. This is probably the best characterized modification of histones, which is carried out under the control of histone acetyltransferases (HATs) and histone deacetylases (HDACs). These enzymes also regulate the activity of a number of transcription factors through acetylation. Increasing evidence links possible dysregulation of these mechanisms in the pathogenesis of diabetes, with important therapeutic implications. Copyright © 2005 John Wiley & Sons, Ltd. [source]


Obesity and type 2 diabetes

NUTRITION BULLETIN, Issue 2 2006
C. Waine
Summary, The rise in obesity , and specifically abdominal obesity , is driving the global increase in type 2 diabetes. Excess visceral fat, the causative factor behind abdominal obesity, is closely linked with ,-cell dysfunction and insulin resistance, two of the key components of type 2 diabetes pathogenesis. Attempts to curb the current abdominal obesity and type 2 diabetes epidemics will require a government-led public health approach, in tandem with a personal approach aimed at helping abdominally obese individuals reduce their cardiovascular and metabolic (cardiometabolic) risk profile. [source]