Faculty Opinions recommendation of Association between coronary vascular dysfunction and cardiac mortality in patients with and without diabetes mellitus.

2013 ◽  
Author(s):  
Juan-Carlos Kaski ◽  
Amelia Carro
Keyword(s):  
Diabetes Mellitus ◽  
Vascular Dysfunction ◽  
Cardiac Mortality

scholarly journals Association Between Coronary Vascular Dysfunction and Cardiac Mortality in Patients With and Without Diabetes Mellitus

Circulation ◽  
2012 ◽  
Vol 126 (15) ◽  
pp. 1858-1868 ◽  
Author(s):  
Venkatesh L. Murthy ◽  
Masanao Naya ◽  
Courtney R. Foster ◽  
Mariya Gaber ◽  
Jon Hainer ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Vascular Dysfunction ◽  
Cardiac Mortality

scholarly journals Ly6C + Inflammatory Monocyte Differentiation Partially Mediates Hyperhomocysteinemia-Induced Vascular Dysfunction in Type 2 Diabetic db/db Mice

2019 ◽  
Vol 39 (10) ◽  
pp. 2097-2119 ◽  
Author(s):  
Pu Fang (方璞) ◽  
Xinyuan Li (李欣源) ◽  
Huimin Shan (单慧敏) ◽  
Jason J. Saredy ◽  
Ramon Cueto ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Bone Marrow Cells ◽  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Underlying Mechanism ◽  
Monocyte Subset ◽  
Monocyte Differentiation ◽  
Inflammatory Monocyte ◽  
M1 Macrophage

Objective: Hyperhomocysteinemia (HHcy) is a potent risk factor for diabetic cardiovascular diseases. We have previously reported that hyperhomocysteinemia potentiates type 1 diabetes mellitus-induced inflammatory monocyte differentiation, vascular dysfunction, and atherosclerosis. However, the effects of hyperhomocysteinemia on vascular inflammation in type 2 diabetes mellitus (T2DM) and the underlying mechanism are unknown. Approach and Results: Here, we demonstrate that hyperhomocysteinemia was induced by a high methionine diet in control mice (homocysteine 129 µmol/L), which was further worsened in T2DM db/db mice (homocysteine 180 µmol/L) with aggravated insulin intolerance. Hyperhomocysteinemia potentiated T2DM-induced mononuclear cell, monocyte, inflammatory monocyte (CD11b + Ly6C + ), and M1 macrophage differentiation in periphery and aorta, which were rescued by folic acid-based homocysteine-lowering therapy. Moreover, hyperhomocysteinemia exacerbated T2DM-impaired endothelial-dependent aortic relaxation to acetylcholine. Finally, transfusion of bone marrow cells depleted for Ly6C by Ly6c shRNA transduction improved insulin intolerance and endothelial-dependent aortic relaxation in hyperhomocysteinemia+T2DM mice. Conclusions: Hyperhomocysteinemia potentiated systemic and vessel wall inflammation and vascular dysfunction partially via inflammatory monocyte subset induction in T2DM. Inflammatory monocyte may be a novel therapeutic target for insulin resistance, inflammation, and cardiovascular complications in hyperhomocysteinemia+T2DM.

Insulin treatment prevents vascular dysfunction in early juvenile alloxan-induced diabetes mellitus

1984 ◽  
Vol 247 (1) ◽  
pp. H132-H138
Author(s):  
S. M. Mueller
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Treatment ◽  
Vascular Dysfunction ◽  
Treated Group ◽  
Diabetic Rats ◽  
Testing Procedures ◽  
Threshold Response ◽  
Sympathetic Function ◽  
Microvascular Pathology ◽  
Juvenile Diabetic

Microvascular pathology and sympathetic autonomic dysfunction have been described early in alloxan-induced diabetic juvenile rats. To determine the longitudinal development of these changes and whether insulin treatment can alter them, vascular and sympathetic function were studied in alloxan-induced (42.5 mg/kg) juvenile diabetic rats and saline-treated controls. The rats were examined 1 and 14 days after induction of diabetes. An insulin-treated group was studied with the 14-day group. Hindquarter perfusion with an artificial solution at constant flow/100 g hindquarter wt was used. After 14 days of diabetes mellitus, the diabetic group showed a significantly depressed response to central ischemia (P less than 0.001), maximal vasoconstriction (P less than 0.02), and maximal dilation (P less than 0.001) compared with both the control and insulin-treated group. The threshold response to norepinephrine did not differ. After 1 day of glucose elevation no differences were present between the control and diabetic animals during any of the testing procedures. These results suggest that severe vascular dysfunction develops early in juvenile-onset alloxan diabetes and that it can be prevented with insulin treatment.

Vascular dysfunction in diabetes mellitus

The Lancet ◽  
1997 ◽  
Vol 350 ◽  
pp. S9-S13 ◽  
Author(s):  
Edward P Feener ◽  
George L King
Keyword(s):  
Diabetes Mellitus ◽  
Vascular Dysfunction

scholarly journals Vascular Dysfunction in Obstructive Sleep Apnea and Type 2 Diabetes Mellitus

Obesity ◽  
2011 ◽  
Vol 19 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Susie Yim-Yeh ◽  
Shilpa Rahangdale ◽  
Anh Tu Duy Nguyen ◽  
Karen E. Stevenson ◽  
Victor Novack ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Obstructive Sleep Apnea ◽  
Type 2 Diabetes Mellitus ◽  
Sleep Apnea ◽  
Vascular Dysfunction ◽  
Obstructive Sleep

scholarly journals Vascular Disease in Diabetic Women: Why Do They Miss the Female Protection?

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Ana Paula Villela Dantas ◽  
Zuleica Bruno Fortes ◽  
Maria Helena Catelli de Carvalho
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Type 2 Diabetes Mellitus ◽  
Vascular Disease ◽  
Vascular Dysfunction ◽  
Protective Effects ◽  
Vascular Protection

Gender plays a pivotal role in the onset as well as in the progression of the cardiovascular disease with a higher morbidity and mortality being detected in men with respect to women. Type 2 Diabetes Mellitus (T2DM) may reduce gender-related differences in the prevalence of cardiovascular disease by fading the vascular protective effects afforded by estrogen in females. This article will discuss the role of sex and sex hormones on the incidence and mechanisms involved in vascular dysfunction associated to T2DM, which might explain why women with T2DM lack the vascular protection.

scholarly journals Ethanolic Extract of Centella asiatica Treatment in the Early Stage of Hyperglycemia Condition Inhibits Glomerular Injury and Vascular Remodeling in Diabetic Rat Model

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Wiwit A. W. Setyaningsih ◽  
Nur Arfian ◽  
Akbar S. Fitriawan ◽  
Ratih Yuniartha ◽  
Dwi C. R. Sari
Keyword(s):  
Diabetes Mellitus ◽  
Vascular Injury ◽  
Rat Model ◽  
Vascular Remodeling ◽  
Kidney Diseases ◽  
Early Stage ◽  
Vascular Dysfunction ◽  
Centella Asiatica ◽  
Control Group ◽  
Glomerular Injury

Background. Diabetes mellitus (DM) is marked by oxidative stress, inflammation, and vascular dysfunction that caused diabetic nephropathy that resulted in end-stage renal disease (ESRD). Vascular dysfunction is characterized by an imbalance in vasoconstrictor and vasodilator agents which underlies the mechanism of vascular injury in DM. Additionally, diminished podocytes correlate with the severity of kidney injury. Podocyturia often precedes proteinuria in several kidney diseases, including diabetic kidney disease. Centella asiatica (CeA) is known as an anti-inflammatory and antioxidant and has neuroprotective effects. This research aimed to investigate the potential effect of CeA to inhibit glomerular injury and vascular remodeling in DM. Methods. The DM rat model was induced through intraperitoneal injection of streptozotocin 60 mg/kg body weight (BW), and then rats were divided into 1-month DM (DM1, n = 5), 2-month DM (DM2, n = 5), early DM concurrent with CeA treatment for 2 months (DMC2, n = 5), and 1-month DM treated with CeA for 1-month (DM1C1, n = 5). The CeA (400 mg/kg BW) was given daily via oral gavage. The control group (Control, n = 5) was maintained for 2 months. Finally, rats were euthanized and kidneys were harvested to assess vascular remodeling using Sirius Red staining and the mRNA expression of superoxide dismutase, podocytes marker, ACE2, eNOS, and ppET-1 using RT-PCR. Results. The DM groups demonstrated significant elevation of glucose level, glomerulosclerosis, and proteinuria. A significant reduction of SOD1 and SOD3 promotes the downregulation of nephrin and upregulation of TRPC6 mRNA expressions in rat glomerular kidney. Besides, this condition enhanced ppET-1 and inhibited eNOS and ACE2 mRNA expressions that lead to the development of vascular remodeling marked by an increase of wall thickness, and lumen wall area ratio (LWAR). Treatment of CeA, especially the DMC2 group, attenuated glomerular injury and showed the reversal of induced conditions. Conclusions. Centella asiatica treatment at the early stage of diabetes mellitus ameliorates glomerulosclerosis and vascular injury via increasing antioxidant enzymes.

Sign in / Sign up

Export Citation Format

Share Document