scholarly journals Shared genetic contribution to type 1 and type 2 diabetes risk

2018 ◽  
Author(s):  
Anthony Aylward ◽  
Joshua Chiou ◽  
Mei-Lin Okino ◽  
Nikita Kadakia ◽  
Kyle J Gaulton
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Genetic Risk ◽  
Islet Function ◽  
Risk Variants ◽  
Association Data ◽  
Shared Risk ◽  
Shared Genetic

AbstractThe role of shared genetic risk in the etiology of type 1 diabetes (T1D) and type 2 diabetes (T2D) and the mechanisms of these effects is unknown. In this study, we generated T1D association data of 15k samples imputed into the HRC reference panel which we compared to T2D association data of 159k samples imputed into 1000 Genomes. The effects of genetic variants on T1D and T2D risk at known loci and genome-wide were positively correlated, which we replicated using data from the UK Biobank and clinically-defined diabetes in the WTCCC. Increased risk of T1D and T2D was correlated with higher fasting insulin and fasting glucose level and decreased birth weight, among T1D- and T2D-specifc correlations, and T1D and T2D associated variants were enriched in regulatory elements for pancreatic, insulin resistance (adipose, CD19+ B cell), and developmental (CD184+ endoderm) cell types. We fine-mapped causal variants at known T1D and T2D loci and found evidence for co-localization at five signals, four of which had same direction of effect, including CENPW and GLIS3. Shared risk variants at GLIS3 and other signals were associated with measures of islet function, while CENPW was associated with early growth, and we identified shared risk variants at GLIS3 in islet accessible chromatin with allelic effects on islet regulatory activity. Our findings support shared genetic risk involving variants affecting islet function as well as insulin resistance, growth and development in the etiology of T1D and T2D.

scholarly journals Shared genetic risk contributes to type 1 and type 2 diabetes etiology

2018 ◽  
Author(s):  
Anthony Aylward ◽  
Joshua Chiou ◽  
Mei-Lin Okino ◽  
Nikita Kadakia ◽  
Kyle J Gaulton
Keyword(s):  
Type 2 Diabetes ◽  
Genetic Risk ◽  
Shared Genetic

1746-P: Obese Youth with Type 1 Diabetes (T1D) Have Worse Hepatic Insulin Resistance (IR) Than Youth with Type 2 Diabetes (T2D)

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1746-P
Author(s):  
PATTARA WIROMRAT ◽  
MELANIE CREE-GREEN ◽  
BRYAN C. BERGMAN ◽  
KALIE L. TOMMERDAHL ◽  
AMY BAUMGARTNER ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Hepatic Insulin Resistance ◽  
Obese Youth

scholarly journals Evaluation of type 2 diabetes genetic risk variants in Chinese adults: findings from 93,000 individuals from the China Kadoorie Biobank

Diabetologia ◽  
2016 ◽  
Vol 59 (7) ◽  
pp. 1446-1457 ◽  
Author(s):  
Wei Gan ◽  
◽  
Robin G. Walters ◽  
Michael V. Holmes ◽  
Fiona Bragg ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Genetic Risk ◽  
Chinese Adults ◽  
Risk Variants ◽  
Genetic Risk Variants

scholarly journals Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status: a potential marker of fetal insulin resistance

2005 ◽  
Vol 82 (6) ◽  
pp. 1162-1168 ◽  
Author(s):  
Yoeju Min ◽  
Clara Lowy ◽  
Kebreab Ghebremeskel ◽  
Beverley Thomas ◽  
Brigid Offley-Shore ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acid ◽  
Essential Fatty Acid ◽  
Fatty Acid Status ◽  
Potential Marker ◽  
Unfavorable Effect ◽  
Acid Status

scholarly journals Genetic Risk Score of 46 Type 2 Diabetes Risk Variants Associates With Changes in Plasma Glucose and Estimates of Pancreatic  -Cell Function Over 5 Years of Follow-Up

Diabetes ◽  
2013 ◽  
Vol 62 (10) ◽  
pp. 3610-3617 ◽  
Author(s):  
E. A. Andersson ◽  
K. H. Allin ◽  
C. H. Sandholt ◽  
A. Borglykke ◽  
C. J. Lau ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Risk Score ◽  
Plasma Glucose ◽  
Genetic Risk ◽  
Cell Function ◽  
Genetic Risk Score ◽  
Pancreatic Cell ◽  
Risk Variants

scholarly journals Gene therapy of type 2 diabetes mellitus: state of art

2019 ◽  
Vol 91 (2) ◽  
pp. 149-152 ◽  
Author(s):  
Yu S Stafeev ◽  
M Yu Menshikov ◽  
Ye V Parfyonova
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Gene Therapy ◽  
Type 2 Diabetes Mellitus ◽  
Metabolic Diseases ◽  
Modern World ◽  
Viral Gene

Type 2 diabetes mellitus (T2DM) and other metabolic diseases are essential links in the structure of morbidity and mortality in the modern world. The accepted strategy for the correction of T2DM and insulin resistance is drug therapy aimed at delivering insulin from the outside, stimulating the secretion of own insulin and reducing the concentration of blood glucose. However, modern studies demonstrate a great potential for the use of gene therapy approaches for the correction of T2DM and insulin resistance. In the present review, the main variants of plasmid gene therapy of T2DM using the genes of adiponectin and type 1 glucagon-like peptide, as well as the main variants of viral gene therapy of T2DM using the genes of type 1 and leptin are considered. T2DM gene therapy is currently not ready to enter into routine clinical practice, but, subject to improvements in delivery systems, it can be a powerful link in combination therapy for diabetes.

Effects of Pterostilbene on Diabetes, Liver Steatosis and Serum Lipids

2020 ◽  
Vol 28 (2) ◽  
pp. 238-252 ◽  
Author(s):  
Saioa Gómez-Zorita ◽  
Iñaki Milton-Laskíbar ◽  
Leixuri Aguirre ◽  
Alfredo Fernández-Quintela ◽  
Jianbo Xiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Animal Models ◽  
Phenolic Compound ◽  
Liver Steatosis ◽  
Positive Effects

: Pterostilbene, a phenolic compound derived from resveratrol, possesses greater bioavailability than its parent compound due to the presence of two methoxyl groups. In this review, the beneficial effects of pterostilbene on diabetes, liver steatosis and dyslipidemia are summarized. Pterostilbene is a useful bioactive compound in preventing type 1 diabetes, insulin resistance and type 2 diabetes in animal models. Concerning type 1 diabetes, the main mechanisms described to justify the positive effects of this phenolic compound are increased liver glycogen content and hepatic glucokinase and phosphofructokinase activities, the recovery of pancreatic islet architecture, cytoprotection and a decrease in serum and pancreatic pro-inflammatory cytokines. As for type 2 diabetes, increased liver glucokinase and glucose-6-phosphatase and decreased fructose-1,6-biphosphatase activities are reported. When insulin resistance is induced by diets, a greater activation of insulin signaling cascade has been reported, increased cardiotrophin-1 levels and liver glucokinase and glucose- 6-phosphatase activities, and a decreased fructose-1,6-biphosphatase activity. Data concerning pterostilbene and liver steatosis are scarce so far, but the reduction in oxidative stress induced by pterostilbene may be involved since oxidative stress is related to the progression of steatosis to steatohepatitis. Finally, pterostilbene effectively reduces total cholesterol, LDL-cholesterol and serum triglyceride levels, while increases HDL-cholesterol in animal models of dyslipidemia.

A Comprehensive Type 1 Diabetes Genetic Risk Score Is Associated with Type 2 Diabetes in the Framingham Heart Study

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1715-P
Author(s):  
SHYLAJA SRINIVASAN ◽  
AARON LEONG ◽  
MIRIAM UDLER ◽  
BIANCA C. PORNEALA ◽  
JAMES B. MEIGS ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Risk Score ◽  
Genetic Risk ◽  
Framingham Heart Study ◽  
Genetic Risk Score ◽  
Heart Study

Animal models of catheter-induced intimal hyperplasia in type 1 and type 2 diabetes and the effects of pharmacologic intervention

2009 ◽  
Vol 87 (1) ◽  
pp. 37-50 ◽  
Author(s):  
D.B. McNamara ◽  
S.N. Murthy ◽  
A.N. Fonseca ◽  
C.V. Desouza ◽  
P.J. Kadowitz ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Animal Models ◽  
Vascular Injury ◽  
Intimal Hyperplasia ◽  
In Vivo Studies ◽  
Impaired Insulin

Diabetes is a complex disorder characterized by impaired insulin formation, release or action (insulin resistance), elevated blood glucose, and multiple long-term complications. It is a common endocrine disorder of humans and is associated with abnormalities of carbohydrate and lipid metabolism. There are two forms of diabetes, classified as type 1 and type 2. In type 1 diabetes, hyperglycemia is due to an absolute lack of insulin, whereas in type 2 diabetes, hyperglycemia is due to a relative lack of insulin and insulin resistance. More than 90% of people with diabetes have type 2 with varied degrees of insulin resistance. Insulin resistance is often associated with impaired insulin secretion, and hyperglycemia is a common feature in both types of diabetes, but failure to make a distinction between the types of diabetes in different animal models has led to confusion in the literature. This is particularly true in relation to cardiovascular disease in the presence of diabetes and especially the response to vascular injury, in which there are major differences between the two types of diabetes. Animal models do not completely mimic the clinical disease seen in humans. Animal models are at best analogies of the pathologic process they are designed to represent. The focus of this review is an analysis of intimal hyperplasia following catheter-induced vascular injury, including factors that may complicate comparisons between different animal models or between in vitro and in vivo studies. We examine the variables, pitfalls, and caveats that follow from the manner of induction of the injury and the diabetic state of the animal. The efficacy of selected antidiabetic drugs in inhibiting the development of the hyperplastic response is also discussed.

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