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.

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.

Magnesium intake, insulin resistance and markers of endothelial function among women

2021 ◽  
pp. 1-9
Author(s):  
Narges Ghorbani Bavani ◽  
Parvane Saneei ◽  
Ammar Hassanzadeh Keshteli ◽  
Ahmadreza Yazdannik ◽  
Ebrahim Falahi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Adhesion Molecule ◽  
Cell Function ◽  
Intercellular Adhesion Molecule ◽  
Model Assessment ◽  
Serum Concentrations ◽  
Homeostasis Model Assessment

Abstract Objective: We investigated the association of dietary Mg intake with insulin resistance and markers of endothelial function among Iranian women. Design: A cross-sectional study. Setting: Usual dietary intakes were assessed using a validated FFQ. Dietary Mg intake was calculated by summing up the amount of Mg in all foods. A fasting blood sample was taken to measure serum concentrations of glycemic indices (fasting plasma glucose and insulin) and endothelial function markers (E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1). Insulin resistance and sensitivity were estimated using the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR), Homeostasis Model Assessment β-cell function (HOMA-β) and quantitative insulin sensitivity check index (QUICKI). Participants: Iranian female nurses (n 345) selected by a multistage cluster random sampling method. Results: The Mg intake across energy-adjusted quartiles was 205 (se 7), 221·4 (se 8), 254·3 (se 7) and 355·2 (se 9) mg/d, respectively. After adjustments for potential confounders, QUICKI level was significantly different across quartiles of Mg intake (Q1: 0·34 (se 0·02), Q2: 0·36 (se 0·01), Q3: 0·40 (se 0·01), and Q4: 0·39 (se 0·02), P = 0·02); however, this association disappeared after considering markers of endothelial function, indicating that this relation might be mediated through endothelial dysfunction. After controlling for all potential confounders, Mg intake was inversely, but not significantly, associated with serum concentrations of sICAM (Q1: 239 (se 17), Q2: 214 (se 12), Q3: 196 (se 12), and Q4: 195 (se 17), P = 0·29). There was no other significant association between dietary Mg intake and other indicators of glucose homoeostasis or endothelial markers. Conclusions: Higher dietary Mg intake was associated with better insulin sensitivity in Iranian females. This linkage was mediated through reduced endothelial dysfunction.

Abstract 3519: Modest Fat Gain Causes Endothelial Dysfunction In Lean Healthy Humans: A Randomized Blinded Controlled Trial

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Abel Romero Corral ◽  
Justo Sierra-Johnson ◽  
Marek Orban ◽  
Apoor S Gami ◽  
Fatima H Sert Kuniyoshi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Weight Loss ◽  
Body Composition ◽  
Weight Gain ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Controlled Trial ◽  
Subcutaneous Fat ◽  
Flow Mediated Dilation

Background: Endothelial dysfunction assessed by flow mediated dilation (FMD) of the brachial artery has been identified as an independent predictor of cardiovascular events. However, whether weight gain impairs endothelial function is unknown. Methods: A randomized blinded controlled-trial to assess the effects of weight gain on endothelial function. After a weight maintenance period supervised by an experience dietitian, volunteers were randomized to gain weight (4 kg) or maintain weight. We recruited lean (BMI 18.5–24.9 kg/m 2 ) healthy volunteers (no diseases, medications and non-smokers) from the community. Using ultrasound, endothelial function was measured by FMD and non-flow mediated dilation (NFMD) of the brachial artery in the early morning (6:30 a.m.). Endothelial function was measured at baseline, after fat gain at 8 weeks and after weight loss at 16 weeks for fat-gainers and at baseline and follow-up (8 weeks) for weight maintainers. Body composition techniques to measure body fat %, such as dual x-ray absorptiometry and abdominal CT scans were performed. Results: We recruited 35 fat-gainers and 8 weight maintainers. Mean age was 29 ± 6 years and 18 (42 %) were women. There were no differences in age, anthropometric and body composition measurements, blood pressure, heart rate or apnea hypopnea index at baseline between both groups. After an average gain of 4 kg, the fat-gainer group significantly increased their total, visceral and subcutaneous fat. Brachial artery FMD and NFMD remained unchanged in weight maintainers. However, it decreaed in fat-gainers (FMD=9.1 ± 3 vs. 7.6 ± 3.2, p=0.003 and NFMD=12.0 ± 4.9 vs. 10.1 ± 6.0, p=0.01), but recovered to baseline after subjects shed the gained weight (basleline vs. recovery: FMD=9.1 ± 3 vs. 9.0 ± 3, p=NS and NFMD =12.0 ± 4.9 vs.12.6 ± 5.0, p=NS). Visceral fat gain, but not subcutaneous fat gain was significantly correlated with the decrease in brachial artery FMD (rho =−0.42, p=0.004 and rho =−0.22, p=0.15, respectively). Conclusions: In lean healthy young subjects, modest weight gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial funcion recovers after weight loss. Viscerar rather than subcutaneous fat predicts endothelial dysfunction.

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&#60;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.

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.

Early experimental obesity is associated with coronary endothelial dysfunction and oxidative stress

2007 ◽  
Vol 292 (2) ◽  
pp. H904-H911 ◽  
Author(s):  
Offer Galili ◽  
Daniele Versari ◽  
Katherine J. Sattler ◽  
Monica L. Olson ◽  
Dallit Mannheim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Microvascular Permeability ◽  
Systemic Oxidative Stress ◽  
Coronary Endothelium ◽  
And Oxidative Stress

Obesity is independently associated with increased cardiovascular risk. However, since established obesity clusters with various cardiovascular risk factors, configuring the metabolic syndrome, the early effects of obesity on vascular function are still poorly understood. The current study was designed to evaluate the effect of early obesity on coronary endothelial function in a new animal model of swine obesity. As to method, juvenile domestic crossbred pigs were randomized to either high-fat/high-calorie diet (HF) or normal chow diet for 12 wk. Coronary microvascular permeability and abdominal wall fat were determined by using electron beam computerized tomography. Epicardial endothelial function and oxidative stress were measured in vitro. Systemic oxidative stress, renin-angiotensin activity, leptin levels, and parameters of insulin sensitivity were evaluated. As a result, HF pigs were characterized by abdominal obesity, hypertension, and elevated plasma lysophosphatidylcholine and leptin in the presence of increased insulin sensitivity. Coronary endothelium-dependent vasorelaxation was reduced in HF pigs and myocardial microvascular permeability increased compared with those values in normal pigs. Systemic redox status in HF pigs was similar to that in normal pigs, whereas the coronary endothelium demonstrated higher content of superoxide anions, nitrotyrosine, and NADPH-oxidase subunits, indicating increased tissue oxidative stress. In conclusion, the current study shows that early obesity is characterized by increased vascular oxidative stress and endothelial dysfunction in association with increased levels of leptin and before the development of insulin resistance and systemic oxidative stress. Vascular dysfunction is therefore an early manifestation of obesity and might contribute to the increased cardiovascular risk, independently of insulin resistance.

Impaired cerebral CO2 vasoreactivity: association with endothelial dysfunction

2006 ◽  
Vol 291 (4) ◽  
pp. H1856-H1861 ◽  
Author(s):  
Shahar Lavi ◽  
Diana Gaitini ◽  
Victor Milloul ◽  
Giris Jacob
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Area Under The Curve ◽  
Healthy Controls ◽  
No Donor

Conflicting data exist on the role of nitric oxide (NO) in cerebral blood flow (CBF) autoregulation. Previous studies involving human and animal subjects seem to indicate that NO involvement is limited to the CO2-dependent mechanism (chemoregulation) and not to the pressure-dependent autoregulation (mechanoregulation). We tested this hypothesis in patients with impaired endothelial function compared with healthy controls. Blood pressure, heart rate, end-tidal Pco2, CBF velocities (CBFV), forearm blood flow, and reactive hyperemia were assessed in 16 patients with diabetes mellitus and/or hypertension and compared with 12 age- and sex-matched healthy controls. Pressure-dependent autoregulation was determined by escalating doses of phenylephrine. CO2 vasoreactivity index was extrapolated from individual slopes of mean CBFV during normocapnia, hyperventilation, and CO2 inhalation. Measurements were repeated after sodium nitroprusside infusion. Indexes of endothelial function, maximal and area under the curve (AUC) of forearm blood flow (FBF) changes, were significantly impaired in patients (maximal flow: 488 ± 75 vs. 297 ± 31%; P = 0.01, AUC ΔFBF: 173 ± 17 vs. 127 ± 11; P = 0.03). Patients and controls showed similar changes in cerebrovascular resistance during blood pressure challenges (identical slopes). CO2 vasoreactivity was impaired in patients compared with controls: 1.19 ± 0.1 vs. 1.54 ± 0.1 cm·s−1·mmHg−1; P = 0.04. NO donor (sodium nitroprusside) offsets this disparity. These results suggest that patients with endothelial dysfunction have impaired CO2 vasoreactivity and preserved pressure-dependent autoregulation. This supports our hypothesis that NO is involved in CO2-dependent CBF regulation alone. CBFV chemoregulation could therefore be a surrogate of local cerebral endothelial function.

P6205Increase in EPA/AA Ratio Predicts Improvement in Endothelial Function in Purified Eicosapentaenoic Acid-Treated Patients

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Fukumoto ◽  
Y Takemoto ◽  
J Yoshikawa ◽  
N Norioka ◽  
T Iguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Eicosapentaenoic Acid ◽  
Brachial Artery ◽  
Multivariate Regression ◽  
Density Lipoprotein ◽  
Intima Media Thickness ◽  
Omega 3 ◽  
Clinical Variables

Abstract Background Omega-3 polyunsaturated fatty acids (n-3 PUFAs) are well-known for preventing cardiovascular disease. Among n-3 PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) play key roles in preventing cardiovascular diseases. However, the effects of n-3 PUFAs have been examined under conditions of simultaneous administration of EPA and DHA in the majority of clinical investigations and the effect of purified EPA is still controversial. EPA has been reported to improve endothelial dysfunction. Although several mechanisms underlying the effects of EPA on endothelial function have been demonstrated such as the modulation of lipid metabolism including increases in high-density lipoprotein (HDL) and/or decreases in triglyceride (TG) levels, decreases in cytokine production, and inhibition of inflammatory processes, the main mechanisms ameliorating endothelial function have not been fully determined. Purpose We sought to clarify the main factors associated with EPA administration that led to improved endothelial function. Methods Fifty-one consecutive patients with hypertriglyceridemia (mean ± SD age, 60±13 years) with no evidence of coronary artery disease (CAD) were prospectively enrolled and administered purified EPA (1800 mg/day). Forty-eight patients who were not administered EPA were enrolled as age- and sex-matched controls. Clinical variables such as body mass index, HbA1c, fasting glucose level, HDL, low-density lipoprotein, TG, systolic blood pressure, diastolic blood pressure, heart rate, interleukin-6, baseline diameter of the brachial artery, intima-media thickness of the brachial artery, and flow-mediated dilation (FMD) were examined before and after 6 months of treatment. Univariate and multivariate regression analyses were performed to examine the associations between FMD changes and clinical variables. Results FMD was significantly improved from 4.16% ± 1.88% to 6.30% ± 2.24% (p<0.0001) in the EPA group. The change in FMD was positively correlated with the change in EPA/arachidonic acid (AA) ratio (r=0.34, p=0.014). The multivariate regression analysis showed that the change in EPA/AA ratio alone was significantly associated with the change in FMD (p=0.010). Conclusions EPA treatment improves endothelial dysfunction in patients with hypertriglyceridemia without evidence of CAD. The change in FMD was associated with the change in EPA/AA ratio alone. These finding suggest that a direct effect of EPA on the endothelium may be the predominant factor ameliorating endothelial function. Acknowledgement/Funding This study was supported, in part, by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan (15K08649).

Insulin resistance and endothelial dysfunction in smokers: effects of vitamin C

2000 ◽  
Vol 279 (3) ◽  
pp. H1172-H1178 ◽  
Author(s):  
Nobutaka Hirai ◽  
Hiroaki Kawano ◽  
Osamu Hirashima ◽  
Takeshi Motoyama ◽  
Yasushi Moriyama ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Vitamin C ◽  
Glucose Tolerance ◽  
Endothelial Function ◽  
Thiobarbituric Acid ◽  
Normal Glucose Tolerance ◽  
Normal Glucose

Cigarette smoking impairs endothelial function and is one of the major risk factors for atherosclerosis and coronary heart disease. Insulin resistance is associated with major risk factors for atherosclerosis. We examined the effects of vitamin C on insulin sensitivity and endothelial function by measuring steady-state plasma glucose (SSPG) and flow-mediated dilation (FMD) of the brachial artery. We studied 16 current smokers with normal glucose tolerance, 15 nonsmokers with impaired glucose tolerance (IGT), and 17 nonsmokers with normal glucose tolerance as controls. Both SSPG and FMD were blunted in smokers and nonsmokers with IGT compared with controls. In smokers, vitamin C decreased SSPG ( P < 0.01 by ANOVA) with decreasing plasma thiobarbituric acid-reactive substances (TBARS) ( P < 0.05 by ANOVA) and improved FMD ( P < 0.05 by ANOVA). Furthermore, vitamin C improved both SSPG ( P < 0.005 by ANOVA) and FMD ( P < 0.05 by ANOVA) in nonsmokers with IGT. SSPG, FMD, or TBARS in controls did not change after vitamin C infusion. There was a significant correlation between SSPG and FMD both in smokers and nonsmokers with IGT, whereas no correlation was observed in controls. In conclusion, both insulin sensitivity and endothelial function were impaired in smokers and nonsmokers with IGT and were improved by vitamin C. Thus increased reactive oxygen species play an important role in the pathogenesis of insulin resistance as well as endothelial dysfunction in smokers and nonsmokers with IGT.

scholarly journals Effects of the green tea polyphenol epigallocatechin-3-gallate on high-fat diet-induced insulin resistance and endothelial dysfunction

2013 ◽  
Vol 305 (12) ◽  
pp. E1444-E1451 ◽  
Author(s):  
Hyun-Ju Jang ◽  
Simone D. Ridgeway ◽  
Jeong-a Kim
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Green Tea ◽  
High Fat Diet ◽  
Reciprocal Relationship ◽  
Tea Polyphenol ◽  
High Fat ◽  
Green Tea Polyphenol

Insulin resistance, a hallmark of metabolic disorders, is a risk factor for diabetes and cardiovascular disease. Impairment of insulin responsiveness in vascular endothelium contributes to insulin resistance. The reciprocal relationship between insulin resistance and endothelial dysfunction augments the pathophysiology of metabolism and cardiovascular functions. The most abundant green tea polyphenol, epigallocatechin-3-gallate (EGCG), has been shown to have vasodilator action in vessels by activation of endothelial nitric oxide synthase (eNOS). However, it is not known whether EGCG has a beneficial effect in high-fat diet (HFD)-induced endothelial dysfunction. Male C57BL/6J mice were fed either a normal chow diet (NCD) or HFD with or without EGCG supplement (50 mg·kg−1·day−1) for 10 wk. Mice fed a HFD with EGCG supplement gained less body weight and showed improved insulin sensitivity. In vehicle-treated HFD mice, endothelial function was impaired in response to insulin but not to acetylcholine, whereas the EGCG-treated HFD group showed improved insulin-stimulated vasodilation. Interestingly, EGCG intake reduced macrophage infiltration into aortic tissues in HFD mice. Treatment with EGCG restored the insulin-stimulated phosphorylation of eNOS, insulin receptor substrate-1 (IRS-1), and protein kinase B (Akt), which was inhibited by palmitate (200 μM, 5 h) in primary bovine aortic endothelial cells. From these results, we conclude that supplementation of EGCG improves glucose tolerance, insulin sensitivity, and endothelial function. The results suggest that EGCG may have beneficial health effects in glucose metabolism and endothelial function through modulating HFD-induced inflammatory response.

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