Vascular Function and Diabetes Mellitus

Author(s):  
Mark A. Creager ◽  
Joshua A. Beckman
2019 ◽  
Vol 8 ◽  
pp. 1549
Author(s):  
Babak Pezeshki ◽  
Ehsan Bahramali ◽  
Amir Ansari ◽  
Aliasghar Karimi ◽  
Mojtaba Frajam ◽  
...  

Background: Diabetes mellitus (DM) is a common metabolic disease worldwide and has many complications. The vascular events are the major complication of DM that have an important effect on mortality and disability. The physical activity (PA) enhances the vascular function by several pathways. The aim of this study was to evaluation of the relationship between PA and vascular diseases in patients with DM.Materials and Methods: This research was performed as the case-control study that was extracted from a prospective epidemiological research study in Iran (PERSIAN). The patients with type 2 DM more than six months defined as case group and the non-DM subjects in control group with ratio 1:2, and both groups were matched in the term of age and sex. The MET score was used to evaluate the level of PA and blood glucose, lipid profile, body mass index, overweight, dyslipidemia, glomerular filtration rate, myocardial infarction (MI), unstable angina, and stroke.Results: Overall, 1242 patients with DM were extracted, and 2484 non-diabetic subjects were investigated. In the case group, 355(28.6 %) and 887(71.4%) were men and women, respectively, the and 710 (28.6%) men and 1774(71.4%) women in control group. The mean MET score was 30 and 40.97 in the DM and non-DM groups, respectively (P˂0.001). The frequency of MI, stroke, and cardiac ischemia were 44 (3.5%), 37 (3%), and 267 (21.5%), respectively in DM group, and 54 (2.2%), 43 (1.7%), and 389 (15.7%), respectively in non-DM group.Conclusion: The incidence of vascular events associated with PA level in patients with DM and adherence to regular PA reduce the vascular events and DM complications. [GMJ.2019;inpress:e1549]


Life Sciences ◽  
2021 ◽  
pp. 119676
Author(s):  
Oleg V. Kornyushin ◽  
Dmitry L. Sonin ◽  
Alexander S. Polozov ◽  
Vitaly V. Masley ◽  
Maria S. Istomina ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 506 ◽  
Author(s):  
Susana Contreras-Duarte ◽  
Lorena Carvajal ◽  
María Jesús Garchitorena ◽  
Mario Subiabre ◽  
Bárbara Fuenzalida ◽  
...  

Gestational diabetes mellitus (GDM) associates with fetal endothelial dysfunction (ED), which occurs independently of adequate glycemic control. Scarce information exists about the impact of different GDM therapeutic schemes on maternal dyslipidemia and obesity and their contribution to the development of fetal-ED. The aim of this study was to evaluate the effect of GDM-treatments on lipid levels in nonobese (N) and obese (O) pregnant women and the effect of maternal cholesterol levels in GDM-associated ED in the umbilical vein (UV). O-GDM women treated with diet showed decreased total cholesterol (TC) and low-density lipoproteins (LDL) levels with respect to N-GDM ones. Moreover, O-GDM women treated with diet in addition to insulin showed higher TC and LDL levels than N-GDM women. The maximum relaxation to calcitonin gene-related peptide of the UV rings was lower in the N-GDM group compared to the N one, and increased maternal levels of TC were associated with even lower dilation in the N-GDM group. We conclude that GDM-treatments modulate the TC and LDL levels depending on maternal weight. Additionally, increased TC levels worsen the GDM-associated ED of UV rings. This study suggests that it could be relevant to consider a specific GDM-treatment according to weight in order to prevent fetal-ED, as well as to consider the possible effects of maternal lipids during pregnancy.


2013 ◽  
Vol 126 (7) ◽  
pp. 471-482 ◽  
Author(s):  
Vaibhav B. Patel ◽  
Nirmal Parajuli ◽  
Gavin Y. Oudit

Diabetes mellitus results in severe cardiovascular complications, and heart disease and failure remain the major causes of death in patients with diabetes. Given the increasing global tide of obesity and diabetes, the clinical burden of diabetes-induced cardiovascular disease is reaching epidemic proportions. Therefore urgent actions are needed to stem the tide of diabetes which entails new prevention and treatment tools. Clinical and pharmacological studies have demonstrated that AngII (angiotensin II), the major effector peptide of the RAS (renin–angiotensin system), is a critical promoter of insulin resistance and diabetes mellitus. The role of RAS and AngII has been implicated in the progression of diabetic cardiovascular complications and AT1R (AngII type 1 receptor) blockers and ACE (angiotensin-converting enzyme) inhibitors have shown clinical benefits. ACE2, the recently discovered homologue of ACE, is a monocarboxypeptidase which converts AngII into Ang-(1–7) [angiotensin-(1–7)] which, by virtue of its actions on the MasR (Mas receptor), opposes the effects of AngII. In animal models of diabetes, an early increase in ACE2 expression and activity occurs, whereas ACE2 mRNA and protein levels have been found to decrease in older STZ (streptozotocin)-induced diabetic rats. Using the Akita mouse model of Type 1 diabetes, we have recently shown that loss of ACE2 disrupts the balance of the RAS in a diabetic state and leads to AngII/AT1R-dependent systolic dysfunction and impaired vascular function. In the present review, we will discuss the role of the RAS in the pathophysiology and treatment of diabetes and its complications with particular emphasis on potential benefits of the ACE2/Ang-(1–7)/MasR axis activation.


2007 ◽  
Vol 56 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Andreas Schäfer ◽  
Ulrike Flierl ◽  
Christian Vogt ◽  
Stefanie Menninger ◽  
Piet Tas ◽  
...  

2014 ◽  
Vol 42 (2) ◽  
pp. 231-238 ◽  
Author(s):  
Kate Geary ◽  
Leslie A. Knaub ◽  
Irene E. Schauer ◽  
Amy C. Keller ◽  
Peter A. Watson ◽  
...  

Our translational research group focuses on addressing the problem of exercise defects in diabetes with basic research efforts in cell and rodent models and clinical research efforts in subjects with diabetes mellitus. CREB (cAMP-response-element-binding protein) regulates cellular differentiation of neurons, β-cells, adipocytes and smooth muscle cells; it is also a potent survival factor and an upstream regulator of mitochondrial biogenesis. In diabetes and cardiovascular disease, CREB protein content is decreased in the vascular media, and its regulation in aberrant in β-cells, neurons and cardiomyocytes. Loss of CREB content and function leads to decreased vascular target tissue resilience when exposed to stressors such as metabolic, oxidative or sheer stress. This basic research programme set the stage for our central hypothesis that diabetes-mediated CREB dysfunction predisposes the diabetes disease progression and cardiovascular complications. Our clinical research programme revealed that diabetes mellitus leads to defects in functional exercise capacity. Our group has determined that the defects in exercise correlate with insulin resistance, endothelial dysfunction, decreased cardiac perfusion and diastolic dysfunction, slowed muscle perfusion kinetics, decreased muscle perfusion and slowed oxidative phosphorylation. Combined basic and clinical research has defined the relationship between exercise and vascular function with particular emphasis on how the signalling to CREB and eNOS [endothelial NOS (nitric oxide synthase)] regulates tissue perfusion, mitochondrial dynamics, vascular function and exercise capacity. The present review summarizes our current working hypothesis that restoration of eNOS/NOS dysfunction will restore cellular homoeostasis and permit an optimal tissue response to an exercise training intervention.


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