Bromocriptine for type 2 diabetes mellitus
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ABSTRACT:
SUBMITTER: Ooi C
PROVIDER: S-EPMC6513609 | biostudies-literature | 2018 Jul
REPOSITORIES: biostudies-literature
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Project description:Objective:Sympathetic nervous system (SNS) overactivity is a risk factor for insulin resistance and cardiovascular disease (CVD). We evaluated the impact of bromocriptine-QR, a dopamine-agonist antidiabetes medication, on elevated resting heart rate (RHR) (a marker of SNS overactivity in metabolic syndrome), blood pressure (BP) and the relationship between bromocriptine-QR's effects on RHR and HbA1c in type 2 diabetes subjects. Design and Subjects:RHR and BP changes were evaluated in this post hoc analysis of data from a randomized controlled trial in 1014 type 2 diabetes subjects randomized to bromocriptine-QR vs placebo added to standard therapy (diet ± ?2 oral antidiabetes medications) for 24 weeks without concomitant antihypertensive or antidiabetes medication changes, stratified by baseline RHR (bRHR). Results:In subjects with bRHR ?70 beats/min, bromocriptine-QR vs placebo reduced RHR by -3.4 beats/min and reduced BP (baseline 130/79; systolic, diastolic, mean arterial BP reductions [mm Hg]: -3.6 [P = .02], -1.9 [P = .05], -2.5 [P = .02]). RHR reductions increased with higher baseline HbA1c (bHbA1c) (-2.7 [P = .03], -5 [P = .002], -6.1 [P = .002] with bHbA1c ?7, >7, ?7.5%, respectively] in the bRHR ?70 group and more so with bRHR ?80 (-4.5 [P = .07], -7.8 [P = .015], -9.9 [P = .005]). Subjects with bRHR <70 had no significant change in RHR or BP. With bHbA1c ?7.5%, %HbA1c reductions with bromocriptine-QR vs placebo were -0.50 (P = .04), -0.73 (P = .005) and -1.22 (P = .008) with bRHR <70, ?70 and ?80, respectively. With bRHR ?70, the magnitude of bromocriptine-QR-induced RHR reduction was an independent predictor of bromocriptine-QR's HbA1c lowering effect. Conclusion:Bromocriptine-QR lowers elevated RHR with concurrent decrease in BP and hyperglycaemia. These findings suggest a potential sympatholytic mechanism contributing to bromocriptine-QR's antidiabetes effect and potentially its previously demonstrated effect to reduce CVD events.
| S-EPMC6947713 | biostudies-literature
Project description:BackgroundType 2 diabetes (T2DM) patients, including those in good glycemic control, have an increased risk of cardiovascular disease (CVD). Maintaining good glycemic control may reduce long-term CVD risk. However, other risk factors such as elevated vascular sympathetic tone and/or endothelial dysfunction may be stronger potentiators of CVD. This study evaluated the impact of bromocriptine-QR, a sympatholytic dopamine D2 receptor agonist, on progression of metabolic disease and CVD in T2DM subjects in good glycemic control (HbA1c ≤ 7.0%).Methods1834 subjects (1219 bromocriptine-QR; 615 placebo) with baseline HbA1c ≤ 7.0% derived from the Cycloset Safety Trial (this trial is registered with ClinicalTrials.gov Identifier: NCT00377676), a 12-month, randomized, multicenter, placebo-controlled, double-blind study in T2DM, were evaluated. Treatment impact upon a prespecified composite CVD endpoint (first myocardial infarction, stroke, coronary revascularization, or hospitalization for angina/congestive heart failure) and the odds of losing glycemic control (HbA1c >7.0% after 52 weeks of therapy) were determined.ResultsBromocriptine-QR reduced the CVD endpoint by 48% (intention-to-treat; HR: 0.52 [0.28-0.98]) and 52% (on-treatment analysis; HR: 0.48 [0.24-0.95]). Bromocriptine-QR also reduced the odds of both losing glycemic control (OR: 0.63 (0.47-0.85), p = 0.002) and requiring treatment intensification to maintain HbA1c ≤ 7.0% (OR: 0.46 (0.31-0.69), p = 0.0002).ConclusionsBromocriptine-QR therapy slowed the progression of CVD and metabolic disease in T2DM subjects in good glycemic control.
| S-EPMC4427775 | biostudies-literature
Project description:Diabetes Mellitus Type 1 miRnome
| PRJEB51173 | ENA
Project description: Not available
| S-EPMC3064029 | biostudies-literature
Project description:In this project, using discovery-based mass spectrometry approach and adopting data-dependent LC-MS/MS, we detected and identified modified peptides in complex clinical plasma samples and developed first-level biomarker verification strategy. Further, using liquid chromatography-multiple reaction monitoring mass spectrometry (LC-MRM-MS) based targeted approach which virtually quantifies irreversible oxidation at any targeted cysteine, we quantified cysteine tri-oxidation in HSA in diabetes patients. Site-specific tri-oxidized HSA could be a potential biomarker of diabetes and provide directive of disease mechanism.
2020-05-26 | PXD012667 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below.
2010-12-18 | GSE26168 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE21321: Blood microRNA profiles and upregulation of hsa-miR-144 in males with type 2 diabetes mellitus. GSE26167: MicroRNA 144 impairs insulin signaling by inhibiting the expression of insulin receptor substrate 1 in Type 2 Diabetes mellitus Refer to individual Series
2010-12-18 | E-GEOD-26168 | biostudies-arrayexpress
Project description:Results Platelets in non-diabetic patients demonstrated miRNA expression profiles comparable to previously published data. The miRNA expression profiles of platelets in diabetics were similar. Statistical analysis unveiled only three miRNAs (miR-377-5p, miR-628-3p, miR-3137) with high reselection probabilities in resampling techniques, corresponding to signatures with only modest discriminatory performance. Functional annotation of predicted targets for these miRNAs pointed towards an influence of diabetes mellitus on mRNA processing. Conclusions/interpretation We did not find any major differences in platelet miRNA profiles between diabetics and non-diabetics. Minor differences pertained to miRNAs associated with mRNA processing. Thus, previously described differences in plasma miRNAs between diabetic and nondiabetic patients cannot be explained by plain changes in the platelet miRNA profile.
2014-03-14 | GSE44093 | GEO
Project description:To evaluate whether serum micoRNAs can be biomarkers for diagnosis of type 1 diabetes mellitus, we analyzed the serum microRNA expression profiles in 6 patients with new-onset type 1 diabetes mellitus and 6 age- and gender-matched healthy controls. A difference was observed in 31 miRNAs between the patients and controls (fold change ≥ 2, P < 0.05)
2017-02-09 | GSE94649 | GEO
Project description:Diabetes can be simply classified into type 1 diabetes mellitus and type 2 diabetes mellitus. Zinc transporter 8 (ZnT8), a novel islet autoantigen, is specifically expressed in insulin-containing secretory granules of ?-cells. Genetic studies show that the genotypes of SLC30A8 can determine either protective or diabetogenic response depending on environmental and lifestyle factors. The ZnT8 protein expression, as well as zinc content in ?-cells, was decreased in diabetic mice. Thus, ZnT8 might participate in insulin biosynthesis and release, and subsequently involved deteriorated ?-cell function through direct or indirect mechanisms in type 1 diabetes mellitus and type 2 diabetes mellitus. From a clinical feature standpoint, the prevalence of ZnT8A is gradiently increased in type 2 diabetes mellitus, latent autoimmune diabetes in adults and type 1 diabetes mellitus. The frequency and epitopes of ZnT8-specific T cells and cytokine release by ZnT8-specific T cells are also different in diabetic patients and healthy controls. Additionally, the response to ZnT8 administration is also different in type 1 diabetes mellitus and type 2 diabetes mellitus. In the present review, we summarize the literature about clinical aspects of ZnT8 in the pathogenesis of diabetes, and suggest that ZnT8 might play a different role between type 1 diabetes mellitus and type 2 diabetes mellitus.
| S-EPMC4931192 | biostudies-literature