Post-Prandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetes

2007 ◽  
pp. 123-137
Author(s):  
Antonio Ceriello
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Endothelial Dysfunction

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

Chronic consumption of an inositol-enriched beverage ameliorates endothelial dysfunction and oxidative stress in type 2 diabetes

2015 ◽  
Vol 18 ◽  
pp. 598-607 ◽  
Author(s):  
Antonio Hernández-Mijares ◽  
Celia Bañuls ◽  
Susana Rovira-Llopis ◽  
Ángeles Álvarez ◽  
Samuel Orden ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
And Oxidative Stress

scholarly journals Histone deacetylase 3 inhibition alleviates type 2 diabetes mellitus-induced endothelial dysfunction via Nrf2

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Shuai Huang ◽  
Gen Chen ◽  
Jia Sun ◽  
Yunjie Chen ◽  
Nan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Histone Deacetylase ◽  
Vascular Endothelium ◽  
Ros Production ◽  
Histone Deacetylase 3

Abstract Background The mechanism underlying endothelial dysfunction leading to cardiovascular disease in type 2 diabetes mellitus (T2DM) remains unclear. Here, we show that inhibition of histone deacetylase 3 (HDAC3) reduced inflammation and oxidative stress by regulating nuclear factor-E2-related factor 2 (Nrf2), which mediates the expression of anti-inflammatory- and pro-survival-related genes in the vascular endothelium, thereby improving endothelial function. Methods Nrf2 knockout (Nrf2 KO) C57BL/6 background mice, diabetic db/db mice, and control db/m mice were used to investigate the relationship between HDAC3 and Nrf2 in the endothelium in vivo. Human umbilical vein endothelial cells (HUVECs) cultured under high glucose-palmitic acid (HG-PA) conditions were used to explore the role of Kelch-like ECH-associated protein 1 (Keap1) –Nrf2–NAPDH oxidase 4 (Nox4) redox signaling in the vascular endothelium in vitro. Activity assays, immunofluorescence, western blotting, qRT-PCR, and immunoprecipitation assays were used to examine the effect of HDAC3 inhibition on inflammation, reactive oxygen species (ROS) production, and endothelial impairment, as well as the activity of Nrf2-related molecules. Results HDAC3 activity, but not its expression, was increased in db/db mice. This resulted in de-endothelialization and increased oxidative stress and pro-inflammatory marker expression in cells treated with the HDAC3 inhibitor RGFP966, which activated Nrf2 signaling. HDAC3 silencing decreased ROS production, inflammation, and damage-associated tube formation in HG-PA-treated HUVECs. The underlying mechanism involved the Keap1–Nrf2–Nox4 signaling pathway. Conclusion The results of this study suggest the potential of HDAC3 as a therapeutic target for the treatment of endothelial dysfunction in T2DM.

scholarly journals Correlation of Uric Acid with Oxidative Stress and Endothelial Dysfunction in Type 2 Diabetes Mellitus

2021 ◽  
Author(s):  
Siva Prasad Palem
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Uric Acid ◽  
Endothelial Dysfunction ◽  
P Value ◽  
Healthy Controls ◽  
Antioxidant Power

Objective: To evaluate the correlation of uric acid with oxidative stress and endothelial dysfunction in type 2 diabetic subjects.Material and Methods: The study included 120 subjects, among when 60 were type 2 diabetes subjects and the remaining 60 were age and gender matched healthy controls. The biochemical parameters, blood glucose, lipid profile, uric acid and homocysteine, were measured by standard kits in an autoanalyzer. Oxidative stress was evaluated by measuring malondialdehyde (MDA) and total antioxidant power by manual methods such as thio-barbituric acid reactive substances and ferric reducing ability of plasma (FRAP). Endothelial dysfunction was assessed by measuring nitric oxide (NO) by the kinetic cadmium method.Results: A significant elevation of triglycerides, low density lipoprotein (LDL), and MDA were observed in the type 2 diabetes mellitus patients while FRAP and NO were significantly reduced compared to the healthy controls. In addition, the uric acid levels had a highly significant correlation with FRAP (r=0.212, p-value=0.020), and moderately significant correlation with triglycerides (r=0.173, p-value=0.057) and homocysteine (r=0.178, p-value=0.051). Uric acid was negatively correlated with MDA and positively correlated with NO, but not statistically significant.Conclusion: Our findings suggest that uric acid may have antioxidant properties since it had a significant positive correlation with FRAP.

scholarly journals The Adiponectin Receptor Agonist AdipoRon Ameliorates Diabetic Nephropathy in a Model of Type 2 Diabetes

2018 ◽  
Vol 29 (4) ◽  
pp. 1108-1127 ◽  
Author(s):  
Yaeni Kim ◽  
Ji Hee Lim ◽  
Min Young Kim ◽  
Eun Nim Kim ◽  
Hye Eun Yoon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Diabetic Nephropathy ◽  
Protein Kinase ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Receptor Agonist ◽  
Intracellular Ca ◽  
Intracellular Pathways

Adiponectin exerts renoprotective effects against diabetic nephropathy (DN) by activating the AMP-activated protein kinase (AMPK)/peroxisome proliferative-activated receptor–α (PPARα) pathway through adiponectin receptors (AdipoRs). AdipoRon is an orally active synthetic adiponectin receptor agonist. We investigated the expression of AdipoRs and the associated intracellular pathways in 27 patients with type 2 diabetes and examined the effects of AdipoRon on DN development in male C57BLKS/J db/db mice, glomerular endothelial cells (GECs), and podocytes. The extent of glomerulosclerosis and tubulointerstitial fibrosis correlated with renal function deterioration in human kidneys. Expression of AdipoR1, AdipoR2, and Ca2+/calmodulin-dependent protein kinase kinase–β (CaMKKβ) and numbers of phosphorylated liver kinase B1 (LKB1)– and AMPK-positive cells significantly decreased in the glomeruli of early stage human DN. AdipoRon treatment restored diabetes-induced renal alterations in db/db mice. AdipoRon exerted renoprotective effects by directly activating intrarenal AdipoR1 and AdipoR2, which increased CaMKKβ, phosphorylated Ser431LKB1, phosphorylated Thr172AMPK, and PPARα expression independently of the systemic effects of adiponectin. AdipoRon-induced improvement in diabetes-induced oxidative stress and inhibition of apoptosis in the kidneys ameliorated relevant intracellular pathways associated with lipid accumulation and endothelial dysfunction. In high-glucose–treated human GECs and murine podocytes, AdipoRon increased intracellular Ca2+ levels that activated a CaMKKβ/phosphorylated Ser431LKB1/phosphorylated Thr172AMPK/PPARα pathway and downstream signaling, thus decreasing high-glucose–induced oxidative stress and apoptosis and improving endothelial dysfunction. AdipoRon further produced cardioprotective effects through the same pathway demonstrated in the kidney. Our results show that AdipoRon ameliorates GEC and podocyte injury by activating the intracellular Ca2+/LKB1-AMPK/PPARα pathway, suggesting its efficacy for treating type 2 diabetes–associated DN.

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