Proinsulin 2 Knockout NOD Mice: A Model for Genetic Variation of Insulin Gene Expression in Type 1 Diabetes

Diabetes ◽  
2002 ◽  
Vol 51 (Supplement 3) ◽  
pp. S489-S493 ◽  
Author(s):  
D. Dubois-Lafforgue ◽  
L. Mogenet ◽  
K. Thebault ◽  
J. Jami ◽  
P. Krief ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type 1 Diabetes ◽  
Genetic Variation ◽  
Nod Mice ◽  
Insulin Gene ◽  
Insulin Gene Expression

scholarly journals Hepatic Insulin Gene Expression as Treatment for Type 1 Diabetes Mellitus in Rats

1997 ◽  
Vol 11 (6) ◽  
pp. 833-837 ◽  
Author(s):  
Patrick Muzzin ◽  
Randy C. Eisensmith ◽  
Kenneth C. Copeland ◽  
Savio L. C. Woo
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Insulin Gene ◽  
Insulin Gene Expression

scholarly journals Antibiotic-induced acceleration of type 1 diabetes alters maturation of innate intestinal immunity

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Xue-Song Zhang ◽  
Jackie Li ◽  
Kimberly A Krautkramer ◽  
Michelle Badri ◽  
Thomas Battaglia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type 1 Diabetes ◽  
Early Life ◽  
System Development ◽  
Nod Mice ◽  
Intestinal Microbiome ◽  
Host Immune System ◽  
Intestinal Immunity ◽  
Immune System Development

The early-life intestinal microbiota plays a key role in shaping host immune system development. We found that a single early-life antibiotic course (1PAT) accelerated type 1 diabetes (T1D) development in male NOD mice. The single course had deep and persistent effects on the intestinal microbiome, leading to altered cecal, hepatic, and serum metabolites. The exposure elicited sex-specific effects on chromatin states in the ileum and liver and perturbed ileal gene expression, altering normal maturational patterns. The global signature changes included specific genes controlling both innate and adaptive immunity. Microbiome analysis revealed four taxa each that potentially protect against or accelerate T1D onset, that were linked in a network model to specific differences in ileal gene expression. This simplified animal model reveals multiple potential pathways to understand pathogenesis by which early-life gut microbiome perturbations alter a global suite of intestinal responses, contributing to the accelerated and enhanced T1D development.

scholarly journals Auto-regulated Hepatic Insulin Gene Expression in Type 1 Diabetic Rats

2001 ◽  
Vol 3 (4) ◽  
pp. 584-590 ◽  
Author(s):  
Ruihuan Chen ◽  
Marcia L. Meseck ◽  
Savio L.C. Woo
Keyword(s):  
Gene Expression ◽  
Diabetic Rats ◽  
Insulin Gene ◽  
Insulin Gene Expression

scholarly journals Genetic Variation in Type 1 Diabetes Reconfigures the 3D Chromatin Organization of T Cells and Alters Gene Expression

Immunity ◽  
2020 ◽  
Vol 52 (2) ◽  
pp. 257-274.e11 ◽  
Author(s):  
Maria Fasolino ◽  
Naomi Goldman ◽  
Wenliang Wang ◽  
Benjamin Cattau ◽  
Yeqiao Zhou ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Type 1 Diabetes ◽  
Genetic Variation ◽  
Chromatin Organization

scholarly journals IFN Regulatory Factors 4 and 8 Expression in the NOD Mouse

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Gilles Besin ◽  
Simon Gaudreau ◽  
Émilie Dumont-Blanchette ◽  
Michael Ménard ◽  
Chantal Guindi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Type 1 Diabetes ◽  
Nod Mice ◽  
Nod Mouse ◽  
Dc Functions ◽  
Gm Csf ◽  
Diabetes Progression ◽  
Islet Inflammation

Dendritic cells (DCs) contribute to islet inflammation and its progression to diabetes in NOD mouse model and human. DCs play a crucial role in the presentation of autoantigen and activation of diabetogenic T cells, and IRF4 and IRF8 are crucial genes involved in the development of DCs. We have therefore investigated the expression of these genes in splenic DCs during diabetes progression in NOD mice. We found that IRF4 expression was upregulated in splenocytes and in splenic CD11c+DCs of NOD mice as compared to BALB/c mice. In contrast, IRF8 gene expression was higher in splenocytes of NOD mice whereas its expression was similar in splenic CD11c+DCs of NOD and BALB/c mice. Importantly, levels of IRF4 and IRF8 expression were lower in tolerogenic bone marrow derived DCs (BMDCs) generated with GM-CSF as compared to immunogenic BMDCs generated with GM-CSF and IL-4. Analysis of splenic DCs subsets indicated that high expression of IRF4 was associated with increased levels of CD4+CD8α−IRF4+CD11c+DCs but not CD4−CD8α+IRF8+CD11c+DCs in NOD mice. Our results showed that IRF4 expression was up-regulated in NOD mice and correlated with the increased levels of CD4+CD8α−DCs, suggesting that IRF4 may be involved in abnormal DC functions in type 1 diabetes in NOD mice.

scholarly journals Basal Insulin Gene Expression Significantly Improves Conventional Insulin Therapy in Type 1 Diabetic Rats

Diabetes ◽  
2002 ◽  
Vol 51 (1) ◽  
pp. 130-138 ◽  
Author(s):  
H. Dong ◽  
J. Altomonte ◽  
N. Morral ◽  
M. Meseck ◽  
S. N. Thung ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Therapy ◽  
Basal Insulin ◽  
Diabetic Rats ◽  
Insulin Gene ◽  
Conventional Insulin Therapy ◽  
Insulin Gene Expression

scholarly journals Gene Expression Analysis of the Pre-Diabetic Pancreas to Identify Pathogenic Mechanisms and Biomarkers of Type 1 Diabetes

2020 ◽  
Vol 11 ◽  
Author(s):  
Linda Yip ◽  
Rebecca Fuhlbrigge ◽  
Reem Alkhataybeh ◽  
C. Garrison Fathman
Keyword(s):  
Gene Expression ◽  
Type 1 Diabetes ◽  
Disease Progression ◽  
Expression Analysis ◽  
Peripheral Blood ◽  
Gene Expression Analysis ◽  
Nod Mice ◽  
Human Pancreas ◽  
Blood Samples

Type 1 Diabetes (T1D) occurs as a result of the autoimmune destruction of pancreatic β-cells by self-reactive T cells. The etiology of this disease is complex and difficult to study due to a lack of disease-relevant tissues from pre-diabetic individuals. In this study, we performed gene expression analysis on human pancreas tissues obtained from the Network of Pancreatic Organ Donors with Diabetes (nPOD), and showed that 155 genes were differentially expressed by ≥2-fold in the pancreata of autoantibody-positive (AA+) at-risk individuals compared to healthy controls. Only 48 of these genes remained changed by ≥2-fold in the pancreata of established T1D patients. Pathway analysis of these genes showed a significant association with various immune pathways. We were able to validate the differential expression of eight disease-relevant genes by QPCR analysis: A significant upregulation of CADM2, and downregulation of TRPM5, CRH, PDK4, ANGPL4, CLEC4D, RSG16, and FCGR2B was confirmed in the pancreata of AA+ individuals versus controls. Studies have already implicated FCGR2B in the pathogenesis of disease in non-obese diabetic (NOD) mice. Here we showed that CADM2, TRPM5, PDK4, and ANGPL4 were similarly changed in the pancreata of pre-diabetic 12-week-old NOD mice compared to NOD.B10 controls, suggesting a possible role for these genes in the pathogenesis of both T1D and NOD disease. The loss of the leukocyte-specific gene, FCGR2B, in the pancreata of AA+ individuals, is particularly interesting, as it may serve as a potential whole blood biomarker of disease progression. To test this, we quantified FCGR2B expression in peripheral blood samples of T1D patients, and AA+ and AA- first-degree relatives of T1D patients enrolled in the TrialNet Pathway to Prevention study. We showed that FCGR2B was significantly reduced in the peripheral blood of AA+ individuals compared to AA- controls. Together, these findings demonstrate that gene expression analysis of pancreatic tissue and peripheral blood samples can be used to identify disease-relevant genes and pathways and potential biomarkers of disease progression in T1D.

scholarly journals Evaluated the Up –regulation in Gene ‎Expression of Hepatic Insulin Gene and ‎Hepatic Insulin Receptor Gene in Type 1 ‎Diabetic Rats Treated with Cuscuta chinesis ‎Lam.‎

2018 ◽  
Vol 26 (4) ◽  
pp. 75-93 ◽  
Author(s):  
Fadia ‎ H. Al-Sultany ◽  
Ali H. Al- Saadi ‎ ◽  
Ibtihal M Al-Husainy
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Serum Insulin ◽  
Receptor Gene ◽  
Diabetic Rats ◽  
Insulin Gene ◽  
Fasting Serum ◽  
Insulin Receptor Gene ◽  
Insulin Gene Expression

        This research was conducted to study the hypoglycemic activity of C. chinesis Lam on type 1 diabetic disease and investigate the  molecular and histological mechanism of  its action .many parameters was investigated , Fasting blood glucose (FBG), Fasting serum insulin,Hepatic Insulin Gene Expression, pancreas Insulin Gene Expression ,Hepatic Insulin  Receptors Gene expression  and histological sections of pancrease and liver.54 Rattus rattus male rats weighting(180 -200g) were divided into 3 groups: A normal control daily administrated with Dw, B Diabetic control daily administrated with Dw  and C  diabetic group daily administrated with 400 mg/Kg body weight of C. chinesis  Lam. methanolic extract, each group consisted of  18 rats and further divided into (3) sub- groups 1 ,2  and 3. According to the period of administration  30, 60 and  90 days respectively. The results showing  the daily administration of 400 mg/Kg body weight of C. chinesis  Lam. methanolic extract for 60 day causing significance  decrease  in FBG and In the other hand each of fasting serum insulin, hepatic Insulin gene expression,pancreas Insulin gene expression and hepatic Insulin receptor gene expression was increased in group C in compare to B group and return all studied parameters involving pancrease and liver texture to the normal state ,which were statically morphologically  not appeared any significant difference from A group .this study concluded that the daily administration type 1 diabetic rats with 400 mg/Kg body weight of C. chinesis  Lam. extract for 60 day was return  fasting serum insulin and FBG to normal value by  upregulated  the gene expression of hepatic INS Gene ,INSR gene , pancreas INS Gene ,regenerate pancreatic beta- cell and returnthe texture of both liver and pancrease to the normal state

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