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 Protein/Lipid Preload Attenuates Glucose-Induced Endothelial Dysfunction in Individuals with Abnormal Glucose Tolerance

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2053
Author(s):  
Domenico Tricò ◽  
Lorenzo Nesti ◽  
Silvia Frascerra ◽  
Simona Baldi ◽  
Alessandro Mengozzi ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Glucose Tolerance ◽  
Endothelial Function ◽  
Plasma Glucose ◽  
Vascular Reactivity ◽  
Strong Predictor ◽  
Reactive Hyperemia ◽  
Postprandial Hyperglycemia ◽  
Oral Glucose ◽  
Postprandial Glycemia

Postprandial hyperglycemia interferes with vascular reactivity and is a strong predictor of cardiovascular disease. Macronutrient preloads reduce postprandial hyperglycemia in subjects with impaired glucose tolerance (IGT) or type 2 diabetes (T2D), but the effect on endothelial function is unknown. Therefore, we examined whether a protein/lipid preload can attenuate postprandial endothelial dysfunction by lowering plasma glucose responses in subjects with IGT/T2D. Endothelial function was assessed by the reactive hyperemia index (RHI) at fasting, 60 min and 120 min during two 75 g oral glucose tolerance tests (OGTTs) preceded by either water or a macronutrient preload (i.e., egg and parmesan cheese) in 22 volunteers with IGT/T2D. Plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucagon, free fatty acids, and amino acids were measured through each test. RHI negatively correlated with fasting plasma glucose. During the control OGTT, RHI decreased by 9% and its deterioration was associated with the rise in plasma glucose. The macronutrient preload attenuated the decline in RHI and markedly reduced postprandial glycemia. The beneficial effect of the macronutrient preload on RHI was proportional to the improvement in glucose tolerance and was associated with the increase in plasma GLP-1 and arginine levels. In conclusion, a protein/lipid macronutrient preload attenuates glucose-induced endothelial dysfunction in individuals with IGT/T2D by lowering plasma glucose excursions and by increasing GLP-1 and arginine levels, which are known regulators of the nitric oxide vasodilator system.

Endothelial function and baroreflex sensitivity according to the oral glucose tolerance test in patients with coronary artery disease and normal fasting glucose levels

2005 ◽  
Vol 109 (4) ◽  
pp. 397-403 ◽  
Author(s):  
Andrzej Wykretowicz ◽  
Przemysław Guzik ◽  
Grzegorz Bartkowiak ◽  
Tomasz Krauze ◽  
Ryszard Kąsinowski ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Endothelial Function ◽  
Fasting Glucose ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Gensini Score ◽  
Normal Fasting Glucose

Endothelial dysfunction and reduced BRS (baroreflex sensitivity) may be present in patients with CAD (coronary artery disease). The normal fasting glucose level does not exclude abnormal glucose metabolism in patients with CAD. The aim of present study was to evaluate endothelial function and BRS according to glucose metabolism in patients with normal fasting plasma glucose and stable CAD subjected to PTCA (percutaneous transluminal coronary angioplasty). Forty-six consecutive patients who underwent elective PTCA were studied (37 men; mean age 56 years). Endothelial function was assessed non-invasively using the arterial vasodilator response to salbutamol (albuterol). BRS was measured using a cross-correlation method. The extent of coronary narrowing was estimated by calculation of the Gensini score. All patients underwent a 75 g OGTT (oral glucose tolerance test). IGT (impaired glucose tolerance) or diabetes was present in approx. 60% of patients. The vasodilator response to salbutamol, as a measure of endothelial dysfunction, was significantly impaired in patients with IGT or diabetes compared with those with normal glucose tolerance (−0.5±1.6% compared with −7.9±2.2; P=0.01). Glucose metabolism and age were significant predictors of endothelial dysfunction (R2=35.2%, P=0.02). BRS did not differ significantly between patients with normal glucose tolerance and those with IGT or diabetes (6.9±1.2 compared with 6.1±0.6 ms/mmHg respectively; P=0.669). BRS was negatively correlated with age (r=−0.34, P=0.021) and the Gensini score (r=−0.34, P=0.022). The significant predictors of BRS were Gensini score, age and past myocardial infarction (R2=37.02%, P=0.002). Patients with established CAD, normal fasting glucose and IGT or diabetes demonstrated impaired endothelial function which did not correlate with the extent of coronary artery involvement. Conversely, BRS in the study population was not affected by glucose metabolism, but showed an interaction with the extent of coronary narrowing.

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 Elevation in blood flow and shear rate prevents hyperglycemia-induced endothelial dysfunction in healthy subjects and those with type 2 diabetes

2015 ◽  
Vol 118 (5) ◽  
pp. 579-585 ◽  
Author(s):  
Arno Greyling ◽  
Tim H. A. Schreuder ◽  
Thijs Landman ◽  
Richard Draijer ◽  
Rebecca J. H. M. Verheggen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Flow ◽  
Shear Rate ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Interaction Effect ◽  
Healthy Subjects ◽  
Local Heating ◽  
Oral Glucose

Hyperglycemia, commonly present after a meal, causes transient impairment in endothelial function. We examined whether increases in blood flow (BF) protect against the hyperglycemia-mediated decrease in endothelial function in healthy subjects and patients with type 2 diabetes mellitus (T2DM). Ten healthy subjects and 10 age- and sex-matched patients with T2DM underwent simultaneous bilateral assessment of brachial artery endothelial function by means of flow-mediated dilation (FMD) using high-resolution echo-Doppler. FMD was examined before and 60, 120, and 150 min after a 75-g oral glucose challenge. We unilaterally manipulated BF by heating one arm between minute 30 and minute 60. Oral glucose administration caused a statistically significant, transient increase in blood glucose in both groups ( P < 0.001). Forearm skin temperature, brachial artery BF, and shear rate significantly increased in the heated arm ( P < 0.001), and to a greater extent compared with the nonheated arm in both groups (interaction effect P < 0.001). The glucose load caused a transient decrease in FMD% ( P < 0.05), whereas heating significantly prevented the decline (interaction effect P < 0.01). Also, when correcting for changes in diameter and shear rate, we found that the hyperglycemia-induced decrease in FMD can be prevented by local heating ( P < 0.05). These effects on FMD were observed in both groups. Our data indicate that nonmetabolically driven elevation in BF and shear rate can similarly prevent the hyperglycemia-induced decline in conduit artery endothelial function in healthy volunteers and in patients with type 2 diabetes. Additional research is warranted to confirm that other interventions that increase BF and shear rate equally protect the endothelium when challenged by hyperglycemia.

Abstract P190: The Associations of Brachial Artery Shear Rate and Endothelial Dysfunction with Age Related Carotid Distensibility

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Dhananjay Vaidya ◽  
Yan Zhang ◽  
Brian G Kral ◽  
Lisa R Yanek ◽  
Lewis C Becker ◽  
...  
Keyword(s):  
Shear Rate ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Reactive Hyperemia ◽  
Hdl Cholesterol ◽  
Lumen Diameter ◽  
Arterial Distensibility ◽  
Age Related ◽  
Increased Risk ◽  
Carotid Distensibility

Loss of carotid artery distensibility (CD) with age portends of clinical cerebrovascular disease. Endothelial dysfunction mediated by impaired nitric oxide vascular dilatation precedes vascular remodeling and age-related stiffening of arteries. However, it is unknown whether endothelial dysfunction contributes to loss of vascular distensibility with age. Methods: We examined 828 asymptomatic healthy subjects in the GeneSTAR family cohort, identified from index cases with early-onset coronary artery disease. We determined mean CD of both common carotid arteries using ultrasound; CD was quantified as the pulsatile change in lumen diameter/diastolic lumen diameter/brachial pulse pressure. Vascular shear rate (SR) was determined in the brachial artery as 4 х maximum blood flow velocity/maximum lumen diameter, and brachial flow mediated dilatation (FMD), a measure of endothelial dysfunction, as % change in diastolic diameter during reactive hyperemia. We tabulated both rest and hyperemic responses by age, sex and race-indexed tertiles of CD generated by quantile regression. Generalized estimating equations (GEE) were used to estimate the family correlation corrected associations of CD with FMD and SR. Results: The sample was 60% female, 40% African American, with mean age 52 (SD 12) years. While SR was significantly associated with higher tertiles of CD, FMD was not (Table). Adjusted for age, sex and race, every 540/s (1 SD) higher of shear rate was significantly associated with a 6.2% higher CD (p = 0.019) but FMD was not associated at all (p = 0.54). This pattern remained after adjustment for LDL and HDL- cholesterol, hypertension, diabetes and smoking (p = 0.03 and 0.95, respectively). Conclusion: Higher vascular shear rate is associated with preserved arterial distensibility indexed for age. FMD is not related to CD. The pathophysiological interpretations of this finding need further study before either CD or vascular shear rate can be used for assessing stoke risk in a population at increased risk for vascular disease.

Managing Cardiovascular Risk in Patients with Type 2 Diabetes – Challenges and Opportunities

2010 ◽  
Vol 6 (4) ◽  
pp. 31
Author(s):  
Lars Rydén ◽  
Linda Mellbin ◽  
Klas Malmberg ◽  
◽  
◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Clinical Trial Data ◽  
Oral Glucose ◽  
Lifestyle Modifications ◽  
Oral Glucose Tolerance Testing ◽  
Coronary Death ◽  
Increased Risk ◽  
Challenges And Opportunities ◽  
Patients With Diabetes ◽  
Multifactorial Approach

The prevalence of diabetes and its associated complications, such as cardiovascular disease (CVD), has increased over recent years and is expected to continue to rise dramatically. People with diabetes have a poor prognosis, with a substantially increased risk of coronary heart disease, coronary death, non-fatal myocardial infarction, stroke, and other vascular deaths compared with non-diabetic subjects. Conversely, studies have also shown that many patients with CVD have undiagnosed dysglycaemia and that already impaired glucose tolerance and newly detected diabetes are associated with an impaired prognosis. Thus, screening for such conditions, preferably with oral glucose tolerance testing, should be performed in all patients with CVD. Guidelines advocate a multifactorial approach to the management of prediabetes, diabetes and CVD. This includes lifestyle modifications as well as targets for glycaemic control, blood pressure, lipids, and other cardiometabolic risk factors. Although clinical trial data have demonstrated that target-driven strategies can improve outcomes in patients with diabetes, the implementation and execution of these regimens in clinical practice needs to improve.

scholarly journals Distinct Effects of a High Fat Diet on Bone in Skeletally Mature and Developing Male C57BL/6J Mice

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1666
Author(s):  
Dean S. Ross ◽  
Tzu-Hsuan Yeh ◽  
Shalinie King ◽  
Julia Mathers ◽  
Mark S. Rybchyn ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Bone Formation ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Age Groups ◽  
Oral Glucose ◽  
Rna Expression ◽  
High Fat ◽  
Mineral Density ◽  
Skeletal Fragility

Increased risks of skeletal fractures are common in patients with impaired glucose handling and type 2 diabetes mellitus (T2DM). The pathogenesis of skeletal fragility in these patients remains ill-defined as patients present with normal to high bone mineral density. With increasing cases of glucose intolerance and T2DM it is imperative that we develop an accurate rodent model for further investigation. We hypothesized that a high fat diet (60%) administered to developing male C57BL/6J mice that had not reached skeletal maturity would over represent bone microarchitectural implications, and that skeletally mature mice would better represent adult-onset glucose intolerance and the pre-diabetes phenotype. Two groups of developing (8 week) and mature (12 week) male C57BL/6J mice were placed onto either a normal chow (NC) or high fat diet (HFD) for 10 weeks. Oral glucose tolerance tests were performed throughout the study period. Long bones were excised and analysed for ex vivo biomechanical testing, micro-computed tomography, 2D histomorphometry and gene/protein expression analyses. The HFD increased fasting blood glucose and significantly reduced glucose tolerance in both age groups by week 7 of the diets. The HFD reduced biomechanical strength, both cortical and trabecular indices in the developing mice, but only affected cortical outcomes in the mature mice. Similar results were reflected in the 2D histomorphometry. Tibial gene expression revealed decreased bone formation in the HFD mice of both age groups, i.e., decreased osteocalcin expression and increased sclerostin RNA expression. In the mature mice only, while the HFD led to a non-significant reduction in runt-related transcription factor 2 (Runx2) RNA expression, this decrease became significant at the protein level in the femora. Our mature HFD mouse model more accurately represents late-onset impaired glucose tolerance/pre-T2DM cases in humans and can be used to uncover potential insights into reduced bone formation as a mechanism of skeletal fragility in these patients.

Sign in / Sign up

Export Citation Format

Share Document