Nephropathy in Type 1 Diabetes: the Role of Genetic Factors

1995 ◽  
Vol 12 (12) ◽  
pp. 1059-1067 ◽  
Author(s):  
T. A. Chowdhury ◽  
S. Kumar ◽  
A. H. Barnett ◽  
S. C. Bain
2008 ◽  
Vol 168 (5) ◽  
pp. 613-617 ◽  
Author(s):  
Stefan Ehehalt ◽  
◽  
Pavle Popovic ◽  
Sergio Muntoni ◽  
Sandro Muntoni ◽  
...  

2020 ◽  
Vol 8 (8) ◽  
pp. 1133
Author(s):  
Keiichiro Mine ◽  
Yasunobu Yoshikai ◽  
Hirokazu Takahashi ◽  
Hitoe Mori ◽  
Keizo Anzai ◽  
...  

Enteroviruses, especially Coxsackie B viruses, are among the candidate environmental factors causative of type 1 diabetes. Host genetic factors have an impact on the development of virus-induced diabetes (VID). Host background, in terms of whether the host is prone to autoimmunity, should also be considered when analyzing the role of target genes in VID. In this review, we describe the genetic susceptibility of the host based on studies in humans and VID animal models. Understanding the host genetic factors should contribute not only to revealing the mechanisms of VID development, but also in taking measures to prevent VID.


2011 ◽  
Vol 57 (1) ◽  
pp. 19-25 ◽  
Author(s):  
T L Kuraeva ◽  
T Iu Shiriaeva ◽  
E V Titovich ◽  
S A Prokof'ev

Type 1 diabetes mellitus (DM1) is characterized by varying levels of morbidity in different populations and its overall increase in the majority of developed countries during the last 30 years. According to IDF, as many as 218,000 new cases of DM1 are registered annually all over the world of whom 75,800 (49%) are children at the age from 0 through 14 years. The yearly incremental increase of DM1 morbidity in this group is estimated at 3%. The marked ethnic variability of DM1 morbidity may be attributed to the different living conditions (environmental factors), population-related differences in the frequency of diabetes-predisposing and protective genetic markers, and the presence of specific markers in different populations. The population-based studies on the occurrence of molecular-genetic markers of DM1 in different ethnic groups confirmed the important role of genetic factors as predictors of diabetes and promoted the understanding of their contribution to the development of the disease in different ethnoses. The results of relevant original and published investigations are discussed.


2013 ◽  
Author(s):  
P. Osborn ◽  
C. A. Berg ◽  
A. E. Hughes ◽  
P. Pham ◽  
D. J. Wiebe

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 317-OR
Author(s):  
BARDEES FODA ◽  
MATTHEW H. FORSBERG ◽  
ASHLEY E. CIECKO ◽  
KEVIN W. MUELLER ◽  
ARON GEURTS ◽  
...  
Keyword(s):  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Gerry K. Schwalfenberg

This paper looks at the environmental role of vitamin D and solar radiation as risk reduction factors in autoimmune disease. Five diseases are considered: multiple sclerosis, type 1 diabetes, rheumatoid arthritis, autoimmune disease of the thyroid, and inflammatory bowel disease. Clinical relevant studies and factors that may indicate evidence that autoimmune disease is a vitamin D-sensitive disease are presented. Studies that have resulted in prevention or amelioration of some autoimmune disease are discussed. An example of the utility of supplementing vitamin D in an unusual autoimmune disease, idiopathic thrombocytic purpura, is presented.


Author(s):  
Tiantian Yue ◽  
Fei Sun ◽  
Faxi Wang ◽  
Chunliang Yang ◽  
Jiahui Luo ◽  
...  

AbstractThe methyl-CpG-binding domain 2 (MBD2) interprets DNA methylome-encoded information through binding to the methylated CpG DNA, by which it regulates target gene expression at the transcriptional level. Although derailed DNA methylation has long been recognized to trigger or promote autoimmune responses in type 1 diabetes (T1D), the exact role of MBD2 in T1D pathogenesis, however, remains poorly defined. Herein, we generated an Mbd2 knockout model in the NOD background and found that Mbd2 deficiency exacerbated the development of spontaneous T1D in NOD mice. Adoptive transfer of Mbd2−/− CD4 T cells into NOD.scid mice further confirmed the observation. Mechanistically, Th1 stimulation rendered the Stat1 promoter to undergo a DNA methylation turnover featured by the changes of DNA methylation levels or patterns along with the induction of MBD2 expression, which then bound to the methylated CpG DNA within the Stat1 promoter, by which MBD2 maintains the homeostasis of Th1 program to prevent autoimmunity. As a result, ectopic MBD2 expression alleviated CD4 T cell diabetogenicity following their adoptive transfer into NOD.scid mice. Collectively, our data suggest that MBD2 could be a viable target to develop epigenetic-based therapeutics against T1D in clinical settings.


2021 ◽  
pp. 193229682110213
Author(s):  
Stuart Chalew ◽  
Alan M. Delamater ◽  
Sonja Washington ◽  
Jayalakshmi Bhat ◽  
Diane Franz ◽  
...  

Achieving normal or near-normal glycemic control as reflected by HbA1c levels in patients with type 1 diabetes (T1D) is important for preventing the development and progression of chronic complications. Despite delineation and dissemination of HbA1c management targets and advances in insulin pharmacology, insulin delivery systems, and glucose monitoring, the majority of children with T1D do not achieve HbA1c goals. In particular, African Americans are more likely not to reach HbA1c goals and have persistently higher HbA1c than Non-Hispanic Whites. Availability of pumps and other technology has not eliminated the disparity in HbA1c. Multiple factors play a role in the persisting racial disparity in HbA1c outcome. The carefully designed application and deployment of new technology to help the patient/family and facilitate the supportive role of the diabetes management team may be able to overcome racial disparity in glycemic outcome and improve patient quality of life.


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