Our results suggested that NKX6.1 expression in β cells was changed in type 2 diabetic subjects, evidenced by significantly increased NKX6.1Nuc-Ins+ and NKX6.1cytIns− cells. This abnormality did not occur more frequently in subjects with a higher risk for T2DM, suggesting that β cell dedifferentiation might be secondary to the pathological changes in T2DM (BMC Endocrine Disorders)
Diabetes News
Category: Genetics
Two decades since the fetal insulin hypothesis: what have we learned from genetics?
In summary, there is now ample evidence to support the idea that variants of certain genes which result in impaired pancreatic beta cell function and reduced insulin secretion contribute to both lower birthweight and higher type 2 diabetes risk in later life when inherited by the fetus (Diabetologia)
Genomic risk score provides predictive performance for type 2 diabetes in the UK biobank
The metaGRS significantly improves T2D prediction ability (Acta Diabetologica)
Glucose metabolism-related gene polymorphisms as the risk predictors of type 2 diabetes
In this review, we have summarized the results reported globally and found that the genetic variants of GCK and OCT3 genes is a risk factor for T2DM while G6PC2 and GCKR genes are controversial in different ethnic groups (Diabetes, Metabolic Syndrome)
Integrating Genetics and the Plasma Proteome to Predict the Risk of Type 2 Diabetes
Studies of the human plasma proteome have started to elucidate its potential for T2D prediction and biomarker discovery (Current Diabetes Reports)
Next steps in the identification of gene targets for type 1 diabetes
The purpose of this review is to provide a view of the future of genomics and other omics approaches in defining the genetic contribution to all stages of risk of type 1 diabetes and the functional impact and clinical implementations of the associated variants (Diabetologia)
Effect of sidt2 Gene on Cell Insulin Resistance and Its Molecular Mechanism
sidt2 knockout can reduce glucose uptake in peripheral tissue under insulin stimulation, which may lead to peripheral tissue insulin resistance by affecting the IRS-1 signal pathway (Journal of Diabetes Research)
What Next After Metformin in Type 2 Diabetes? Selecting the Right Drug for the Right Patient
This study identified patients’ phenotypic characteristics that may have the potential to influence individual treatment response. Accounting for these characteristics in clinical treatment decisions may facilitate individualised prescribing by being able to select the right drug for the right patient (Diabetes Therapy)
Economics of Genetic Testing for Diabetes
CEAs have shown that genetic testing for monogenic diabetes diagnosis can be cost-effective or cost-saving and should guide insurers to consider broader coverage of these tests, which would lead to accurate and timely diagnosis and impact treatment and clinical outcomes (Current Diabetes Reports)
A variant of the glucose transporter gene SLC2A2 modifies the glycaemic response to metformin therapy in recently diagnosed type 2 diabetes
The variant rs8192675 in the SLC2A2 gene (C allele) is associated with an improved glucose response to metformin monotherapy during the first year after diagnosis in type 2 diabetes (Diabetologia)
A Type 1 Diabetes Genetic Risk Score Predicts Progression of Islet Autoimmunity and Development of Type 1 Diabetes in Individuals at Risk
The T1D GRS independently predicts progression to T1D and improves prediction along T1D stages in autoantibody-positive relatives (Diabetes Care)
MC1568 improves insulin secretion in islets from type 2 diabetes patients and rescues β-cell dysfunction caused by Hdac7 upregulation
HDAC7 inhibition protects β-cells from mitochondrial dysfunction and apoptosis, and increases glucose-stimulated insulin secretion in islets from human T2D donors. Our study supports specific HDAC7 inhibitors as novel options in the treatment of T2D (Acta Diabetologica)
The Role of Epigenetics in Type 1 Diabetes
Epigenomics remains in its infancy, and we anticipate further studies will define how the interaction of genetic and non-genetic effects induces tissue-specific destruction and enhances our ability to predict, and possibly even modify that process (Current Diabetes Reports)
Sox5 regulates beta-cell phenotype and is reduced in type 2 diabetes
We suggest that human islets in T2D display changes reminiscent of dedifferentiation and highlight SOX5 as a regulator of β-cell phenotype and function (Nature Communications)
Relative contribution of type 1 and type 2 diabetes loci to the genetic etiology of adult-onset, non-insulin-requiring autoimmune diabetes
LADA is genetically closer to T1D than T2D, although the genetic load of T1D risk alleles is less than childhood-onset T1D, particularly at the major histocompatibility complex region, potentially accounting for the later disease onset. Our results show that the genetic spectrum of T1D extends into adult-onset diabetes, where it can clinically masquerade as T2D (BMC Medicine)
Heritable components of the human fecal microbiome are associated with visceral fat
Our results provide novel insights into the role of the fecal microbiota in cardio-metabolic disease with clear potential for prevention and novel therapies (Genome Biology)
Epigenomic alterations contribute to obesity-associated diabetes
Epigenomic alterations that are associated with inflammation and type 2 diabetes (Karolinska Institutet)
Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes
Our study is one of the first pharmacogenetic studies in the field of T2D, employing a recall-by-genotype design. It demonstrated that the effect of melatonin on glucose metabolism is dependent upon genotype. Although yet to be proven, carriers of the MTNR1B risk variant are likely to have lower cAMP levels in pancreatic β cells. In view of this, incretin-based therapy, which amplifies cAMP signaling in β cells, may be particularly well suited for these patients (Cell Metabolism)
Forkhead box transcription factor 1: role in the pathogenesis of diabetic cardiomyopathy
In this review, we focus on the FOXO1 pathway and its role in various processes that have been related to DCM, such as metabolism, oxidative stress, endothelial dysfunction, inflammation and apoptosis (Cardiovascular Diabetology)
CLOCK gene variation is associated with incidence of type-2 diabetes and cardiovascular diseases in type-2 diabetic subjects: dietary modulation in the PREDIMED randomized trial
We report for the first time an association between a CLOCK polymorphism and stroke in T2D subjects, suggesting that core clock genes may significantly contribute to increased CVD risk in T2D (Cardiovascular Diabetology)
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