The pathogenic variants in the development of endothelial dysfunction of blood vessels among adolescents with obesity

2015 ◽  
Vol 9 (4) ◽  
pp. 0-0
Author(s):  
Черная ◽  
N. Chernaya ◽  
Маскова ◽  
G. Maskova ◽  
Дадаева ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Essential Hypertension ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Metabolic Disorders ◽  
Reactive Hyperemia ◽  
Diabetes Type 2 ◽  
Systemic Blood Pressure ◽  
The Body ◽  
Moderate Increase

Patients and methods. The authors have conducted clinical, functional and laboratory examination of 104 adolescents aged 11-18 years with a primary abdominal obesity type. It was additionally studied the reaction of the brachial artery in the process of conducting endothelial test with reactive hyperemia and calculated of percentage flow-mediated dilation (%FMD). Results. In 66% (n=67) cases it was identified endothelial dysfunction vessel (EDV) among adolescents on the basis of positive endothelial samples (FMD<10%). A further analysis was performed among children with dysfunction of endothelium of the brachial artery. The children were divided into 2 groups: children with essential hypertension and EDV and children without essential hypertension and EDV. Adolescents with essential hypertension had a moderate increase in the percentage content of fat mass (M=31,4±4,7%) and metabolic disorders in the blood are recorded with a frequency: hyperglycemia – 16,6%, ВЕСТНИК НОВЫХ МЕДИЦИНСКИХ ТЕХНОЛОГИЙ – 2015 – № 4 Электронный журнал Библиографическая ссылка: Маскова Г.С., Черная Н.Л., Дадаева О.Б. Патогенетические варианты развития дисфункции эндотелия сосудов у подростков с ожирением // Вестник новых медицинских технологий. Электронное издание. 2015. №4. Публикация 2-4. URL: http://www.medtsu.tula.ru/VNMT/Bulletin/E2015-4/5216.pdf (дата обращения: 18.11.2015). DOI:12737/14921 hypercholesterolemia – 4%, hyperinsulinemia – 27% and insulin resistance – 17%. Children without essential hypertension were characterized by significantly more pronounced metabolic disorders in the blood. In particular, hyperglycemia was reported among 33% of adolescents (p=0,04), hypercholesterolemia among 33% (p=0,04), hyperinsulinemia- 45% (p=0,041) and insulin resistance among 30% (p=0,042). Metabolic disorders of blood were registered at a higher percentage of body fat in the body (M=39,45±4,4%). Conclusion. The results analysis of the selected groups allows to reveal a predominant factor that causes dysfunction of endothelium among adolescents with obesity (high systemic blood pressure or hyperinsulinemia), as well as to determine the pathogenetic variants of further progress obesity: the development essential hypertension or increase metabolic disorders with the formation of diabetes type 2.

Abstract P432: Racial Differences In Endothelial Function And Insulin Sensitivity

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Catharine Couch ◽  
Nikki Bush ◽  
Tanja Dudenbostel ◽  
Barbara Gower
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Steady State ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Reactive Hyperemia ◽  
Health Concern ◽  
Steady State Serum

Racial disparities in health outcomes continue to be a significant public health concern and African Americans (AA) are disproportionately burdened by several risk factors for cardiovascular disease. Endothelial dysfunction has been shown to be a predictor of CVD and metabolic factors, including insulin resistance, are associated with endothelial dysfunction. Compared to EA, AA have impaired endothelial function and are more insulin resistant (less insulin sensitive). However, it remains unclear how insulin resistance may contribute to endothelial dysfunction in AA and EA. The purpose of the present study was to evaluate the relationship between insulin sensitivity and endothelial function in AA and EA. It was hypothesized that insulin sensitivity would be associated with endothelial function in both AA and EA. Skeletal muscle insulin sensitivity was measured by hyperinsulinemic-euglycemic glucose clamp technique in 112 lean, overweight, and obese AA and EA adults without diabetes. Insulin was infused at 120 mU/m 2 /min for 3 hours and an infusion of 20% dextrose was adjusted to maintain blood glucose at the fasting level. Insulin sensitivity (10 -4 .dL.kg -1 .min -1 /(μU/mL)) was defined as M/(G x ΔI), where M is steady state glucose infusion rate, G is steady state serum glucose concentration, and ΔI is the difference between basal and steady state serum insulin concentrations. M was adjusted for total lean body mass which was measured by dual-energy X-ray absorptiometry (DXA). Endothelial function was assessed by percent change in flow-mediated brachial artery dilatation (FMD). Changes in brachial artery diameter during reactive hyperemia were measured using ultrasound. Increased blood flow was induced via blood pressure cuff around the forearm, with a 5-minute inflation at 50 mmHg above the subject’s systolic blood pressure. Brachial arterial flow was determined using a pulsed-Doppler signal at baseline and 10-15 seconds after cuff release. Arterial diameter was measured at end-diastolic phase from super-VHS recordings. For reactive hyperemia response, measurements with the 5 largest diameters were averaged and the percent increase from baseline was determined as FMD. A total of 55 AA and 57 EA were included in the analysis. Mean insulin sensitivity was 4.89 in AA and 7.97 in EA (p < .0001) and mean FMD was 10.69 in AA and 10.14 in EA (p = .595). Linear regression analysis indicated a significant relationship between insulin sensitivity and endothelial function in AA but not in EA (p= .005 and p= .5, respectively). These results suggest that insulin sensitivity may play a role in determining endothelial function in AA.

Essential hypertension, metabolic disorders, and insulin resistance

1991 ◽  
Vol 121 (4) ◽  
pp. 1274-1282 ◽  
Author(s):  
Eleuterio Ferrannini ◽  
Andrea Natali
Keyword(s):  
Insulin Resistance ◽  
Essential Hypertension ◽  
Metabolic Disorders

scholarly journals A new early diagnostic criterion for endothelial dysfunction in men

2017 ◽  
Vol 95 (7) ◽  
pp. 642-647
Author(s):  
Irina A. Khripun ◽  
M. N. Morgunov ◽  
S. V. Vorobyev ◽  
I. I. Belousov ◽  
M. I. Kogan
Keyword(s):  
Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Reactive Hyperemia ◽  
Vascular Complications ◽  
Pathological Process ◽  
The Difference ◽  
Reliable Marker ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Endothelial dysfunction (ED) triggers vascular complications in many diseases, including diabetes mellitus. Currently existing methods for detection of ED do not ensure early diagnostics of the pathological process. We examined 168 men with type 2 diabetes mellitus. ED was studied by ultrasound assessment of arterial vasoreactivity of the brachial artery and determination of biochemical ED markers. Based on manifestations of reactive hyperemia, the patients were divided into groups according to the presence or absence of ED. It was shown that 23.2%of the patients exhibiting normal endothelium-dependent vasodilation in response to the reactive hyperemia test had s.582 + 353_379del polymorphism of the endothelial nitric oxide synthase gene. We also demonstrated that the time till maximum vasodilatation in these patients was 33.3% longer, on the average, than in men who did not have such polymorphism. The slowdown of the maximum response of endothelium-dependent vasodilation was associated with increased levels of ED proteomic markers VCAM-1 and ICAM-1 in 27% and 22.9% of the cases respectively. Thus, we showed for the first time that the time till maximum vasodilation is a more reliable marker of ED than the difference between the diameters of the brachial artery during reactive hyperemia test expressed in percentage.

ENDOTHELIAL DYSFUNCTION AND STRUCTURAL VASCULAR CHANGES IN THE BRACHIAL ARTERY OF PATIENTS WITH ESSENTIAL HYPERTENSION

2000 ◽  
Vol 18 ◽  
pp. S183
Author(s):  
L. Ghiadoni ◽  
Y. Huang ◽  
A. Magagna ◽  
S. Buralli ◽  
S. Taddei ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Vascular Changes

scholarly journals Role of immunological disorders, endothelial dysfunction and hemostatic disorders in the genesis of arterial hypertension in the metabolic syndrome

2020 ◽  
Vol 22 (2) ◽  
pp. 221-230
Author(s):  
E. I. Polozova ◽  
E. V. Puzanova ◽  
A. A. Seskina
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Immune Cells ◽  
Metabolic Disorders ◽  
Vascular Wall ◽  
Immunological Disorders ◽  
Hemostatic Disorders

Mortality from diseases of the circulatory system is a challenge for the modern health care. Arterial hypertension (AH) mostly contributes to development of cardiovascular complications. It often proceeds against the background of metabolic disorders. Pathogenesis of hypertension is currently being considered a multifactorial disease. Pathogenesis of hypertension certainly has distinct features in presence of metabolic disorders,. Therefore, it is relevant to summarize current literature on the role of immunological disorders, endothelial dysfunction and hemostatic disorders in AH genesis during metabolic syndrome (MS). Most authors agree with existence of several mechanisms that determine relationships between AH and insulin resistance. Development of hypertension in MS patients with is a consequence of immunometabolic processes. Abdominal obesity is an important component of MS. It is associated with chronic inflammation of visceral adipose tissue, its excessive infiltration by immune cells, and increased production of adipokines and cytokines (TNFα, IL-6) with hypertension. AH is associated with a significant increase in T cells, that mediate endothelial dysfunction (ED) and provide a link between hypertension and subsequent atherosclerosis. T lymphocytes trigger a cascade of reactions. IL-17 is the end product of these events It is involved not only in increasing blood pressure, but also contributes to the development of vascular wall stiffness in АН patients. Thus, the relationship between several types of immune cells leads to inflammatory reactions, including those of vascular wall, initiating endothelial dysfunction. Chronic non-specific inflammation in MS, supported by the cytokine system, is a triggering mechanism for ED progression. Excessive production of endothelin-1 and inhibition of nitric oxide production are the classic markers of ED. Immune damage leads to imbalance in the production of vasoconstrictor and vasodilating substances, proliferative and antiproliferative factors in endothelium. It was shown that ED is an integral aspect of the insulin resistance syndrome in pathogenesis of arterial hypertension associated with metabolic disorders, and contributes to its worsening, increased vascular reactivity and further AH development. According to modern studies, it has been shown that excessive synthesis of pro-inflammatory cytokines introduces disturbances in the system of vascular hemostasis. When studying the effects of metabolic disorders upon hemostatic system, we may conclude that activation of fibrinolytic and plasma chains occurs in the same way for both men and women, with small gender characteristics of individual components. The rheological properties of the blood are also changed with developing MS. Systematization of the available literature data on the issue under study can serve as a basis for determining prognostic criteria of hypertension progression and risk of thrombotic complications.

scholarly journals Endothelial Function in Women with and without a History of Glucose Intolerance in Pregnancy

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Shireen Brewster ◽  
John Floras ◽  
Bernard Zinman ◽  
Ravi Retnakaran
Keyword(s):  
Shear Rate ◽  
Endothelial Dysfunction ◽  
Glucose Tolerance ◽  
Endothelial Function ◽  
Glucose Intolerance ◽  
Brachial Artery ◽  
Reactive Hyperemia ◽  
Oral Glucose ◽  
Oral Glucose Tolerance Testing ◽  
In Pregnancy

Background/Aims. Gestational diabetes mellitus (GDM) and milder gestational impaired glucose tolerance (GIGT) identify women who are at risk of developing cardiovascular disease. Endothelial dysfunction, as indicated by impaired flow-mediated dilatation (FMD) on brachial artery ultrasound, is an early marker of vascular disease. Thus, we sought to evaluate endothelial function in women with and without recent glucose intolerance in pregnancy.Methods. One-hundred and seventeen women underwent oral glucose tolerance testing (OGTT) in pregnancy, enabling stratification into those with normal gestational glucose tolerance (n=59) and those with GDM or GIGT (n=58). 6 years postpartum, they underwent a repeat of OGTT and brachial artery FMD studies, enabling assessment of FMD and 4 secondary vascular measures: FMD after 60 seconds (FMD60), baseline arterial diameter, peak shear rate, and reactive hyperemia.Results. There were no differences between the normal gestational glucose tolerance and GDM/GIGT groups in FMD (mean 8.5 versus 9.3%,P=0.61), FMD60(4.1 versus 5.1%,P=0.33), baseline diameter (3.4 versus 3.4 mm,P=0.66), peak shear rate (262.6 versus 274.8 s−1,P=0.32), and reactive hyperemia (576.6 versus 496.7%,P=0.07). After covariate adjustment, there were still no differences between the groups.Conclusion. Despite their long-term cardiovascular risk, women with glucose intolerance in pregnancy do not display endothelial dysfunction 6 years postpartum.

scholarly journals A Pilot Study of External Counterpulsation on Reactive Hyperemia, Levels of Glycemia and Metabolic Parameters in Type 2 Diabetes Mellitus

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A464-A465
Author(s):  
Caroline Wei Shan Hoong ◽  
Maudrene Tan ◽  
Shih Ling Kao ◽  
Eric Yin Hao Khoo
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Lipid Profile ◽  
Fasting Glucose ◽  
Reactive Hyperemia ◽  
Metabolic Parameters ◽  
Vibration Sense ◽  
Duration Of Diabetes

Abstract Introduction: External counter-pulsation (ECP) involves cuff inflation over the lower extremities to generate sheer stress, thereby improving endothelial function and anginal symptoms in coronary artery disease. Endothelial dysfunction is also involved in the pathogenesis of T2DM. We hypothesized that 1) ECP will be associated with an improvement in endothelial function in T2DM as measured by peripheral artery tonometry, and 2) explored whether this would vary with different dose and frequency regimens. A shorter or less intensive regimen could potentially reduce cost and improve patient compliance if a similar therapeutic response is achieved. Methods: This single-center prospective study in a tertiary institute in Singapore involving 46 adults with T2DM of HbA1c between 7 to 10%, who were randomly assigned to receive 35 sessions of ECP at different regimens and duration. Subjects in arm 1 received 1-hour daily sessions 5x per week for 7 consecutive weeks, subjects in arm 2 received 0.5-hour sessions 5x per week for 7 consecutive weeks, and subjects in arm 3 received 1-hour sessions 3x per week for 12 consecutive weeks. Endothelial function was evaluated by reactive hyperemia index (RHI) via peripheral arterial tonometry measured at the start, midpoint and end of study. Other secondary outcomes included fasting glucose, homeostatic model assessment of insulin resistance (HOMA-IR), HbA1c, blood pressure, lipid profile, weight and vibration sense. Results: 42 subjects completed the 35-session course of ECP. Mean age was 56.1±9.3 years, duration of diabetes 8.8±4.7 years, baseline RHI 2.0 (1.3–3.7) and baseline HOMA-IR was 3.1 (0.5–18.7). All regimes of ECP were well-tolerated. There was no change in RHI across all 3 regimens of ECP individually or collectively at the end of the study (ΔRHI +0.01%, p=0.458). Glycaemic markers of fasting glucose, HbA1c and HOMA-IR, as well as blood pressure, lipid profile, weight and vibration sense also remained unchanged at endpoint. Subgroup analysis showed a significant improvement in RHI (ΔRHI +20.6%, p=0.0178) in 7 subjects with more severe endothelial dysfunction (defined by RHI&lt;1.67) at baseline who had a trend to having a longer duration of diabetes, however there was no improvement in fasting glucose, HbA1c, HOMA-IR or metabolic parameters in this group. Conclusion: ECP did not show a beneficial effect on endothelial function, glycemic control or metabolic parameters in this South-East Asian population with T2DM at any of the three regimens. This may partly be explained by less severe endothelial dysfunction and less insulin resistance in our population at baseline. Future studies of ECP may investigate its potential benefits in a larger population of T2DM with more severe endothelial dysfunction, higher insulin resistance and/or longer duration of diabetes at baseline.

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