PubMed Journals Articles About "A Study Of SIMPONI® To Arrest Beta-cell Loss In Type 1 Diabetes" RSS

20:41 EST 16th February 2019 | BioPortfolio

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Showing "Study SIMPONI Arrest Beta cell Loss Type Diabetes" PubMed Articles 1–25 of 89,000+

The transcription factor STAT6 plays a critical role in promoting beta cell viability and is depleted in islets of individuals with type 1 diabetes.

In type 1 diabetes, selective beta cell loss occurs within the inflamed milieu of insulitic islets. This milieu is generated via the enhanced secretion of proinflammatory cytokines and by the loss of anti-inflammatory molecules such as IL-4 and IL-13. While the actions of proinflammatory cytokines have been well-studied in beta cells, the effects of their anti-inflammatory counterparts have received relatively little attention and we have addressed this.

MicroRNA-24 promotes pancreatic beta cells toward dedifferentiation to avoid endoplasmic reticulum stress-induced apoptosis.

Current research indicates that beta cell loss in type 2 diabetes may be attributed to beta cell dedifferentiation rather than apoptosis; however, the mechanisms by which this occurs remain poorly understood. Our previous study demonstrated that elevation of microRNA-24 (miR-24) in a diabetic setting caused beta cell dysfunction and replicative deficiency. In this study, we focused on the role of miR-24 in beta cell apoptosis and dedifferentiation under endoplasmic reticulum (ER) stress conditions. We found...

Novel minor HLA DR associated antigens in type 1 diabetes.

Type 1 diabetes is an autoimmune disease leading to insulin deficiency. Autoantibodies to beta cell proteins are already present in the asymptomatic phase of type 1 diabetes. Recent findings have suggested a number of additional minor autoantigens in patients with type 1 diabetes. We have established luciferase immunoprecipitation systems (LIPS) for anti-MTIF3, anti-PPIL2, anti-NUP50 and anti-MLH1 and analyzed samples from 500 patients with type 1 diabetes at onset of clinical disease and 200 healthy indivi...

TGF-beta/TGF-beta RII/CLC-3 axis promotes cognitive disorders in diabetes.

Transforming growth factor beta (TGF-beta) and Chloride channel-3 (CLC-3) are critical for inflammatory response, cellular proliferation and apoptosis in hippocampus neurons. However, the relationship between CLC-3 and TGF-beta/TGF-beta Receptor II (RII) pathway in diabetic encephalopathy (DE) is unknown. In this study, both diabetes rat model and diabetes cell model were employed to elucidate the mechanisms involved. The increased expressions of CLC-3 and TGF- beta RII with cognitive impairment were observ...

Activation of GLP-1 receptor signalling alleviates cellular stresses and improves beta cell function in a mouse model of Wolfram syndrome.

Loss of functional beta cells results in a gradual progression of insulin insufficiency in Wolfram syndrome caused by recessive WFS1 mutations. However, beta cell dysfunction in Wolfram syndrome has yet to be fully characterised, and there are also no specific treatment recommendations. In this study, we aimed to characterise beta cell secretory defects and to examine the potential effects of a glucagon-like peptide-1 (GLP-1) receptor agonist on diabetes in Wolfram syndrome.

The effects of incretin-based therapies on beta-cell function and insulin resistance in type 2 diabetes: a systematic review and network meta-analysis combining 360 trials.

To evaluate the comparative effects of incretin-based therapies, including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dipeptidyl peptidase-4 inhibitors (DPP-4Is), on beta-cell function and insulin resistance in patients with type 2 diabetes mellitus (T2DM).

A proteomic signature that reflects pancreatic beta-cell function.

Proteomics has the potential to enhance early identification of beta-cell dysfunction, in conjunction with monitoring the various stages of type 2 diabetes onset. The most routine method of assessing pancreatic beta-cell function is an oral glucose tolerance test, however this method is time consuming and carries a participant burden. The objectives of this research were to identify protein signatures and pathways related to pancreatic beta-cell function in fasting blood samples.

Bone fragility in type 1 diabetes and type 2 diabetes.

Diabetes mellitus causes hyperglycemia due to resistance to insulin action in peripheral organs in addition to progressive loss of β-cell function, thus it is involved in the development and progression of diabetic microangiopathy(retinopathy, nephropathy, and neuropathy). In addition, abnormalities of bone metabolism is regarded as a chronic complication related to both type 1 diabetes and type 2 diabetes. Accumulating evidence suggests that type 1 diabetes patients had decreased bone mineral density(BMD)...

Patient and family expectations of beta-cell replacement therapies in type 1 diabetes.

New methods of beta-cell replacement have been developed to maintain excellent glycemic control, improve quality of life, and even eliminate insulin injections in patients with type 1 diabetes mellitus (T1DM). Previously, we demonstrated that being insulin-free is the strongest motivation for accepting a newly developed therapy. Multiple allogeneic islet transplantations with immunosuppression using a human donor is the best option to be insulin-free, but the necessity for immunosuppression and donor shorta...

Prevention and reversal of Type 2 diabetes: highlights from a symposium at the 2018 Diabetes UK Annual Professional Conference.

This symposium covers the gamut of Type 2 diabetes prevention, reversing established Type 2 diabetes, population-level delivery of weight loss programmes and personal insights into achieving and retaining substantial weight loss.

Beta Cell Functional Adaptation and Dysfunction in Insulin Resistance and the Role of Chronic Kidney Disease.

Beta cells are central in the pathophysiology of diabetes, since their functional adaptation maintains euglycemia in insulin-resistant individuals and beta cell dysfunction is required for the clinical picture of frank diabetes. The pathophysiological mechanisms driving compensation and decompensation are incompletely understood and little is known about the influence of chronic kidney disease (CKD) on beta cell function.

Extracellular matrix and the maintenance and loss of peripheral immune tolerance in autoimmune insulitis.

There is a growing appreciation that the extracellular matrix (ECM) contributes to both the maintenance of immune tolerance in healthy tissues and to its loss at sites of autoimmunity. Here, we review recent literature on the role of ECM and particularly the glycosaminoglycans hyaluronan and heparan sulfate in the development of autoimmune, type 1 diabetes (T1D). Data from transplant models suggest that healthy islets are embedded within an intact ECM that supports beta-cell homeostasis and provides physica...

Insulin mutations impair beta-cell development in a patient-derived iPSC model of neonatal diabetes.

Insulin gene mutations are a leading cause of neonatal diabetes. They can lead to proinsulin misfolding and its retention in endoplasmic reticulum (ER). This results in increased ER-stress suggested to trigger beta-cell apoptosis. In humans, the mechanisms underlying beta-cell failure remain unclear. Here we show that misfolded proinsulin impairs developing beta-cell proliferation without increasing apoptosis. We generated induced pluripotent stem cells (iPSCs) from people carrying insulin () mutations, eng...

Differential methylation of the type 2 diabetes susceptibility locus KCNQ1 is associated with insulin sensitivity and is predicted by CpG site specific genetic variation.

Epigenetic mechanisms regulate gene expression and may influence the pathogenesis of type 2 diabetes through the loss of insulin sensitivity. The aims of this study were to measure variation in DNA methylation at the type 2 diabetes locus KCNQ1 and assess its relationship with metabolic measures and with genotype.

Inappropriate glucagon and GLP-1 secretion in individuals with long-standing type 1 diabetes: effects of residual C-peptide.

Recent studies have demonstrated that residual beta cells may be present in some people with long-standing type 1 diabetes, but little is known about the potential impact of this finding on alpha cell function and incretin levels. This study aimed to evaluate whether insulin microsecretion could modulate glucagon and glucagon-like peptide-1 (GLP-1) responses to a mixed meal tolerance test (MMTT).

Effects of proinsulin misfolding on β-cell dynamics, differentiation and function in diabetes.

ER stress due to proinsulin misfolding has an important role in the pathophysiology of rare forms of permanent neonatal diabetes (PNDM) and probably also of common type 1 (T1D) and type 2 diabetes (T2D). Accumulation of misfolded proinsulin in the ER stimulates the unfolded protein response (UPR) that may eventually lead to apoptosis through a process called the terminal UPR. However, the β-cell ER has an incredible ability to cope with accumulation of misfolded proteins; therefore, it is not clear whether...

Crestal Bone Loss Around Submerged and Non-Submerged Dental Implants in Individuals with Type-2 Diabetes Mellitus: A 7-Year Prospective Clinical Study.

In establishing an evidence-based rationale for the optimal use of implant therapy in patients with type 2 diabetes mellitus (T2DM), it is essential to first understand the impact of glycemic control on early healing and the success of dental implants. The objective of this study was to evaluate crestal bone loss (CBL) and stability around submerged and non-submerged dental implants in Saudi patients with well- and poorly-controlled type 2 diabetes mellitus (T2DM).

The discovery of novel predictive biomarkers and early-stage pathophysiology for the transition from gestational diabetes to type 2 diabetes.

Gestational diabetes mellitus (GDM) affects up to 20% of pregnancies, and almost half of the women affected progress to type 2 diabetes later in life, making GDM the most significant risk factor for the development of future type 2 diabetes. An accurate prediction of future type 2 diabetes risk in the early postpartum period after GDM would allow for timely interventions to prevent or delay type 2 diabetes. In addition, new targets for interventions may be revealed by understanding the underlying pathophysi...

MicroRNA-182-5p contributes to the protective effects of thrombospondin 1 against lipotoxicity in INS-1 cells.

The dysfunction of beta cells serves an important role in the pathogenesis of type 2 diabetes mellitus (T2DM). An improved understanding of the molecular mechanisms underlying beta cell mass and failure will be useful for identifying novel approaches toward preventing and treating this disease. Recent studies have indicated that free fatty acids (FFAs) can cause beta cell dysfunction. In the present study, palmitate (Pal) was used as a FFA and its functions on cell viability and apoptosis were detected. MTT...

Progression of Hearing Loss in the Aging Population: Repeated Auditory Measurements in the Rotterdam Study.

We quantified changes in the auditory acuity of 675 aging adults (mean age 71.1 years, 52.0% female, mean follow-up 4.4 years ± 0.2) of an ongoing cohort study with a pure-tone audiogram and a speech-in-noise test. Generalized estimating equation models were used to study the association between hearing loss and the progression with age, sex, education, cognition, BMI, blood pressure, having type 2 diabetes mellitus, cholesterol ratio, smoking and alcohol consumption. The mean progression of hearing loss w...

Growth arrest and DNA-damage-inducible 45 beta (GADD45β) deletion suppresses testosterone-induced prostate hyperplasia in mice.

Growth arrest and DNA-damage-inducible 45 beta (GADD45β) is a member of the gene family associated with cell growth control, apoptosis, and DNA damage repair. The aim of present study was to determine the potential effects of GADD45β deletion on prostate hyperplasia progression.

β Cell Dysfunction in Type 2 Diabetes: Drained of Energy?

Type 2 diabetes is a progressive disorder, but exactly how the progression occurs remains unknown. In this issue of Cell Metabolism, Zhang et al. (2019) present evidence that diabetes, via hyperglycemia, leads to aberrant insertion of a mitochondrial ion channel in the plasma membrane, rendering it leaky to key intracellular signaling molecules with resultant suppression of insulin secretion.

Early administration of dapagliflozin preserves pancreatic beta-cell mass through a legacy effect in type 2 diabetic mice.

The preservation of pancreatic β-cell mass is an essential factor in the onset and development of type 2 diabetes mellitus. Recently, sodium-glucose co-transporter 2 inhibitors have been launched as anti-hyperglycemic agents, and their organ-protective effects are attracting attention. They are also reported to have favorable effects on the preservation of pancreatic β-cell mass, but the appropriate timing for the administration of sodium-glucose co-transporter 2 inhibitors is obscure.

Increased formations of neutrophil extracellular traps are associated with gut leakage in the patients with type 1 diabetes but not type 2 diabetes.

The aims of this study were to investigate the association of formation of neutrophil extracellular traps (NETs) with gut leakage not only in type 1 diabetes (T1D) but also in type 2 diabetes (T2D).

Comorbidity Type and Health Care Costs in Type 2 Diabetes: A Retrospective Claims Database Analysis.

Previous studies suggest that the type and combination of comorbidities may impact diabetes care, but their cost implications are less clear. This study characterized how diabetes patients' health care utilization and costs may vary according to comorbidity type classified on the basis of the Piette and Kerr framework.

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