scholarly journals Inhibition of Protein Kinase Cβ Does Not Improve Endothelial Function in Type 2 Diabetes

2010 ◽  
Vol 95 (8) ◽  
pp. 3783-3787 ◽  
Author(s):  
Joshua A. Beckman ◽  
Allison B. Goldfine ◽  
Alison Goldin ◽  
Adnan Prsic ◽  
Sora Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Healthy Subjects ◽  
Vascular Dysfunction ◽  
Endothelial Damage ◽  
Markers Of Inflammation ◽  
Resistance Vessels ◽  
Healthy Control ◽  
And Oxidative Stress

Context: Antagonism of protein kinase Cβ (PKCβ) restores endothelial function in experimental models of diabetes and prevents vascular dysfunction in response to hyperglycemia in healthy humans. Objective: We tested the hypothesis that PKCβ antagonism would improve vascular function in subjects with type 2 diabetes compared with healthy control subjects. Design: The effect of PKCβ was evaluated in a randomized, placebo-controlled, double-blinded crossover trial. Setting: The study was performed in the outpatient setting of a university medical center. Participants: Thirteen subjects with type 2 diabetes without evidence of cardiovascular disease and 15 healthy control subjects were recruited via newspaper advertisement. Intervention: Subjects underwent a randomized, double-blind, crossover, placebo-controlled trial of the selective PKCβ antagonist ruboxistaurin mesylate. Subjects received each treatment for 14 d. Main Outcome Measure: Endothelium-dependent and endothelium-independent vasodilation of forearm resistance vessels was measured with mercury-in-silastic, strain-gauge plethysmography during intraarterial administration of methacholine chloride and verapamil, respectively. Markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress were measured after each treatment. Results: Endothelium-dependent vasodilation of forearm resistance vessels was attenuated in diabetic subjects when compared with healthy subjects (P = 0.001). Endothelium-independent vasodilation did not differ between groups (P value not significant). Ruboxistaurin did not significantly change endothelium-dependent or endothelium-independent vasodilation or blood-based markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress in either diabetic or healthy subjects. Conclusion: Endothelial dysfunction of forearm resistance vessels was not improved by 2 wk of selective PKCβ inhibition in patients with diabetes. These results suggest that PKCβ does not contribute significantly to vascular dysfunction in otherwise healthy patients with type 2 diabetes.

scholarly journals Serum leptin concentration in patients with type 2 diabetes

2015 ◽  
Vol 28 (4) ◽  
pp. 236-240
Author(s):  
Arleta Malecha-Jedraszek ◽  
Agata Burska ◽  
Beata Matyjaszek-Matuszek ◽  
Helena Donica
Keyword(s):  
Type 2 Diabetes ◽  
Healthy Subjects ◽  
Control Group ◽  
Early Type ◽  
Anthropometric Parameters ◽  
Markers Of Inflammation ◽  
Gender And Age ◽  
Healthy Control ◽  
Positive Correlations

AbstractWith the increasing importance of early type 2 diabetes (DM2) and obesity detection, it is useful to reevaluate leptin role in these conditions. Our study aimed at investigating circulating leptin concentrations in a group of patients with DM2, and at assessing in detail whether leptin concentrations correlate with selected biochemical, clinical parameters and markers of systemic inflammation in patients with DM2 and in healthy volunteers. In our work, we analysed samples and data drawn from 71 patients aged 61.4 ± 11.7 years, who have been diagnosed with type 2 diabetes, as well as from a healthy control group (HC) consisting of 51 healthy subjects with a mean age of 57.8 ± 13.7 years. Therein, the concentration of leptin in the DM2 patients was significantly higher than in the HC (p < 0.01), with median value of 16.59 (IQR 8.58-33.39) ng/ml in the DM2, vs median value of 6.66 (IQR 4.52-21.40) ng/ml in the HC. In the analysis of variance, higher leptin concentrations were revealed in the DM2 group as compared to the HC, and this figure remained significant after adjusting for gender and age (p < 0.001). Moreover, it was independent of HOMA-IR (p = 0.003). However, the differences in leptin levels between the groups disappeared when additional adjustments for anthropometric parameters (BMI, waist circumference) were applied (p = 0.088). Beyond the aforementioned, significant positive correlations were found in the DM 2 group between leptin level and CRP (r=0.256; p < 0.05) and IL-6 (r = 0.345; p < 0.01). Among the selected variables, only gender and BMI were included in the predictive model explaining the variability of leptin, and, in total, were responsible for 72.6% of the original variation of the studied adipocytokine. The results of this study have led to conclusion that leptin may participate in the complex pathogenesis of DM2 and be a predictor of the development of this disease. As higher concentrations of leptin coexist with obesity, and this situation correlates positively with markers of inflammation (CRP, IL-6), leptin level, hence, should be considered in the pathogenesis of DM2.

scholarly journals Effects of glucose control on arterial stiffness in patients with type 2 diabetes mellitus and hypertension: An observational study

2017 ◽  
Vol 46 (1) ◽  
pp. 284-292 ◽  
Author(s):  
Sangah Chang ◽  
Jihyun Kim ◽  
Taeseo Sohn ◽  
Hyunshik Son ◽  
Jungmin Lee
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Arterial Stiffness ◽  
Hba1c Level ◽  
Augmentation Index ◽  
Markers Of Inflammation ◽  
And Oxidative Stress

Objective We evaluated the association of glucose control with changes in arterial stiffness, inflammatory markers, and oxidative stress markers. Methods Sixty-four patients with uncontrolled type 2 diabetes mellitus (glycated hemoglobin [HbA1c] ≥ 9%) and hypertension were enrolled in this study. The patients were divided into two groups based on their post-treatment HbA1c level: HbA1c ≤ 7% (well-controlled group, n = 28) and HbA1c > 7% (uncontrolled group, n = 36). The pulse wave velocity, augmentation index, and markers of inflammation and oxidative stress were measured and analyzed. Results The patients’ mean baseline HbA1c level was 11.7%. There were no differences in any baseline parameters between the two groups except the duration of diabetes. The mean HbA1c level was significantly lower at 12 weeks in the well-controlled than uncontrolled group (6.1% vs. 9.0%, respectively), but there were no significant differences in the pulse wave velocity (0.33 ± 0.95 vs. 0.36 ± 1.44 m/s), aortic augmentation index (5.1 ± 8.3 vs. 0.7 ± 11.6), or markers of inflammation and oxidative stress. Conclusions Short-term glycemic control did not influence the arterial stiffness in patients with type 2 diabetes mellitus and hypertension.

Alpha-1-Antichymotrypsin: a Common Player for Type 2 Diabetes and Alzheimer's Disease

2020 ◽  
Vol 16 ◽  
Author(s):  
Nataly Guzmán-Herrera ◽  
Viridiana C. Pérez-Nájera ◽  
Luis A. Salazar-Olivo
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Type 2 Diabetes ◽  
Alzheimer's Disease ◽  
Regulatory Networks ◽  
Therapeutic Strategies ◽  
Oxidative Stresses ◽  
Bibliographic Search ◽  
And Oxidative Stress

Background: Numerous studies have shown a significant association between type 2 diabetes mellitus (T2D) and Alzheimer's disease (AD), two pathologies affecting millions of people worldwide. Chronic inflammation and oxidative stress are two conditions common to these diseases also affecting the activity of the serpin alpha-1-antichymotrypsin (ACT), but a possible common role for this serpin in T2D and AD remains unclear. Objective: To explore the possible regulatory networks linking ACT to T2D and AD. Materials and Methods: A bibliographic search was carried out in PubMed, Med-line, Open-i, ScienceDirect, Scopus and SpringerLink for data indicating or suggesting association among T2D, AD, and ACT. Searched terms like “alpha-1-antichymotrypsin”, “type 2 diabetes”, “Alzheimer's disease”, “oxidative stress”, “pro-inflammatory mediators” among others were used. Moreover, common therapeutic strategies between T2D and AD as well as the use of ACT as a therapeutic target for both diseases were included. Results: ACT has been linked with development and maintenance of T2D and AD and studies suggest their participation through activation of inflammatory pathways and oxidative stress, mechanisms also associated with both diseases. Likewise, evidences indicate that diverse therapeutic approaches are common to both diseases. Conclusion: Inflammatory and oxidative stresses constitute a crossroad for T2D and AD where ACT could play an important role. In-depth research on ACT involvement in these two dysfunctions could generate new therapeutic strategies for T2D and AD.

scholarly journals Novel Soy Germ Pasta Improves Endothelial Function, Blood Pressure, and Oxidative Stress in Patients With Type 2 Diabetes: Figure 1

Diabetes Care ◽  
2011 ◽  
Vol 34 (9) ◽  
pp. 1946-1948 ◽  
Author(s):  
Carlo Clerici ◽  
Elisabetta Nardi ◽  
Pier Maria Battezzati ◽  
Stefania Asciutti ◽  
Danilo Castellani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Endothelial Function ◽  
And Oxidative Stress

scholarly journals MicroRNAs and Oxidative Stress: An Intriguing Crosstalk to Be Exploited in the Management of Type 2 Diabetes

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 802
Author(s):  
Teresa Vezza ◽  
Aranzazu M. de Marañón ◽  
Francisco Canet ◽  
Pedro Díaz-Pozo ◽  
Miguel Marti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Signaling Pathways ◽  
Current Knowledge ◽  
Critical Role ◽  
Cell Dysfunction ◽  
Non Coding Rnas ◽  
And Oxidative Stress ◽  
Molecular Crosstalk

Type 2 diabetes is a chronic disease widespread throughout the world, with significant human, social, and economic costs. Its multifactorial etiology leads to persistent hyperglycemia, impaired carbohydrate and fat metabolism, chronic inflammation, and defects in insulin secretion or insulin action, or both. Emerging evidence reveals that oxidative stress has a critical role in the development of type 2 diabetes. Overproduction of reactive oxygen species can promote an imbalance between the production and neutralization of antioxidant defence systems, thus favoring lipid accumulation, cellular stress, and the activation of cytosolic signaling pathways, and inducing β-cell dysfunction, insulin resistance, and tissue inflammation. Over the last few years, microRNAs (miRNAs) have attracted growing attention as important mediators of diverse aspects of oxidative stress. These small endogenous non-coding RNAs of 19–24 nucleotides act as negative regulators of gene expression, including the modulation of redox signaling pathways. The present review aims to provide an overview of the current knowledge concerning the molecular crosstalk that takes place between oxidative stress and microRNAs in the physiopathology of type 2 diabetes, with a special emphasis on its potential as a therapeutic target.

scholarly journals GTP Cyclohydrolase I Gene Polymorphisms Are Associated with Endothelial Dysfunction and Oxidative Stress in Patients with Type 2 Diabetes Mellitus

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e108587 ◽  
Author(s):  
Pawel P. Wolkow ◽  
Wladyslaw Kosiniak-Kamysz ◽  
Grzegorz Osmenda ◽  
Grzegorz Wilk ◽  
Beata Bujak-Gizycka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Gene Polymorphisms ◽  
Gtp Cyclohydrolase I ◽  
And Oxidative Stress ◽  
I Gene

Postprandial Dysmetabolism and Oxidative Stress in Type 2 Diabetes: Pathogenetic Mechanisms and Therapeutic Strategies

2015 ◽  
Vol 35 (5) ◽  
pp. 968-1031 ◽  
Author(s):  
Barbara Sottero ◽  
Simona Gargiulo ◽  
Isabella Russo ◽  
Cristina Barale ◽  
Giuseppe Poli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Therapeutic Strategies ◽  
Pathogenetic Mechanisms ◽  
And Oxidative Stress
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