scholarly journals CLINICAL SIGNIFICANCE OF INSULIN RESISTANCE SYNDROME IN DEVELOPMENT OF ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH PRIMARY GOUT

2012 ◽  
Vol 67 (2) ◽  
pp. 60-63
Author(s):  
N. N. Kushnarenko ◽  
A. V. Govorin ◽  
O. A. Shcherbakova ◽  
S. G. Sotnikova ◽  
O. V. Ivanitskaya
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Carbohydrate Metabolism ◽  
Clinical Significance ◽  
Clinical Course ◽  
Insulin Resistance Syndrome ◽  
Close Link ◽  
Chronic Gout ◽  
Primary Gout

Endothelial function has been studied in 175 males with primary gout. It has been established that incidence of endothelial dysfunction in patients with primary gout was associated with the clinical course and was marked most of all in patients who had a chronic gout. The correlations found between the parameters of endothelial dysfunction and impaired carbohydrate metabolism suggest close link and coordination between the above processes which contribute greatly to development and progress of atherosclerosis in such patients.

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.

The role of insulin and the adipocytokines in regulation of vascular endothelial function

2004 ◽  
Vol 107 (6) ◽  
pp. 519-532 ◽  
Author(s):  
Stuart A. RITCHIE ◽  
Marie-Ann EWART ◽  
Colin G. PERRY ◽  
John M. C. CONNELL ◽  
Ian P. SALT
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Insulin Signalling ◽  
Direct Effects ◽  
Paracrine Factors ◽  
Vascular Integrity ◽  
Beneficial Effects ◽  
Glucose Homoeostasis ◽  
No Bioavailability

Vascular integrity in the healthy endothelium is maintained through the release of a variety of paracrine factors such as NO (nitric oxide). Endothelial dysfunction, characterized by reduced NO bioavailability, is associated with obesity, insulin resistance and Type II diabetes. Insulin has been demonstrated to have direct effects on the endothelium to increase NO bioavailability. Therefore altered insulin signalling in the endothelium represents a candidate mechanism underlying the association between insulin resistance and endothelial dysfunction. In recent years, it has become apparent that insulin sensitivity is regulated by the adipocytokines, a group of bioactive proteins secreted by adipose tissue. Secretion of adipocytokines is altered in obese individuals and there is increasing evidence that the adipocytokines have direct effects on the vascular endothelium. A number of current antidiabetic strategies have been demonstrated to have beneficial effects on endothelial function and to alter adipocytokine concentrations in addition to their effects on glucose homoeostasis. In this review we will explore the notion that the association between insulin resistance and endothelial dysfunction is accounted for by adipocytokine action on the endothelium. In addition, we examine the effects of weight loss, exercise and antidiabetic drugs on adipocytokine availability and endothelial function.

Effects of glucagon-like peptide-1 on endothelial function in type 2 diabetes patients with stable coronary artery disease

2004 ◽  
Vol 287 (6) ◽  
pp. E1209-E1215 ◽  
Author(s):  
Thomas Nyström ◽  
Mark K. Gutniak ◽  
Qimin Zhang ◽  
Fan Zhang ◽  
Jens Juul Holst ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Healthy Subjects ◽  
Stable Coronary Artery Disease ◽  
Artery Disease ◽  
Type 2 Diabetic ◽  
Diabetes Patients

GLP-1 stimulates insulin secretion, suppresses glucagon secretion, delays gastric emptying, and inhibits small bowel motility, all actions contributing to the anti-diabetogenic peptide effect. Endothelial dysfunction is strongly associated with insulin resistance and type 2 diabetes mellitus and may cause the angiopathy typifying this debilitating disease. Therefore, interventions affecting both endothelial dysfunction and insulin resistance may prove useful in improving survival in type 2 diabetes patients. We investigated GLP-1's effect on endothelial function and insulin sensitivity (SI) in two groups: 1) 12 type 2 diabetes patients with stable coronary artery disease and 2) 10 healthy subjects with normal endothelial function and SI. Subjects underwent infusion of recombinant GLP-1 or saline in a random crossover study. Endothelial function was measured by postischemic FMD of brachial artery, using ultrasonography. SI [in (10−4 dl·kg−1·min−1)/(μU/ml)] was measured by hyperinsulinemic isoglycemic clamp technique. In type 2 diabetic subjects, GLP-1 infusion significantly increased relative changes in brachial artery diameter from baseline FMD(%) (3.1 ± 0.6 vs. 6.6 ± 1.0%, P < 0.05), with no significant effects on SI (4.5 ± 0.8 vs. 5.2 ± 0.9, P = NS). In healthy subjects, GLP-1 infusion affected neither FMD(%) (11.9 ± 0.9 vs. 10.3 ± 1.0%, P = NS) nor SI (14.8 ± 1.8 vs. 11.6 ± 2.0, P = NS). We conclude that GLP-1 improves endothelial dysfunction but not insulin resistance in type 2 diabetic patients with coronary heart disease. This beneficial vascular effect of GLP-1 adds yet another salutary property of the peptide useful in diabetes treatment.

scholarly journals The influence of insulin resistance and disturbances of carbohydrate metabolism in the acute period of myocardial infarction

2011 ◽  
Vol 57 (2) ◽  
pp. 9-13 ◽  
Author(s):  
L V Kvitkova ◽  
T S Elenskaia ◽  
O P Blagoveshchenskaia ◽  
S F Zinchuk ◽  
V G Zinchuk ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Carbohydrate Metabolism ◽  
Coronary Arteries ◽  
Clinical Course ◽  
Functional Class ◽  
Immunoreactive Insulin ◽  
Normal Sensitivity ◽  
The Relationship ◽  
Successful Prevention

This work was designed to study parameters of carbohydrate metabolism and insulin resistance (IR) in patients presenting with myocardial infarction (MI) and elucidate their relation to MI complications. Special attention was given to the relationship between disturbances of carbohydrate metabolism (DCM), the clinical course of myocardial infarction in the acute and cicatrization phases, characteristics of coronary arteries in the patients with and without diabetes mellitus (groups 2 and 1 respectively). Insulin resistance was documented in 83.2% of the patients. Multiple lesions in the coronary arteries were shown to be directly related to the immunoreactive insulin (IRI) level (r=0.277; p=0.0008) and HOMA index (r=0.304; p=0.0001). They were more common in patients with IR (86%; p<0.001). The clinical course of MI was more frequently complicated by early post-infarction angina, MI relapses, and heart failure (Killip functional class II) in the patients presenting with a combination of IR and DCM than in those showing normal sensitivity to insulin regardless of the characteristics of carbohydrate metabolism. It is concluded that the detection and correction of insulin resistance and disturbances of carbohydrate metabolism are the indispensable prerequisites for the successful prevention of myocardial infarction.

Endothelial Dysfunction and Subclincal Atherosclerosis in Insulin Resistance Syndrome

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 690-690
Author(s):  
Akira Satoh ◽  
Hidehiro Matsuoka ◽  
Shuji Iida ◽  
Kei Fukami ◽  
Seiya Okuda ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Mean Arterial Pressure ◽  
Endothelial Dysfunction ◽  
Healthy Subjects ◽  
Structural Changes ◽  
Subclinical Atherosclerosis ◽  
Insulin Resistance Syndrome ◽  
Large Artery ◽  
Apparently Healthy

68 Insulin resistance syndrome, which constitutes obesity, hypertension, impaired glucose tolerance, and low high density lipoprotein is closely associated with cardiovascular events. Impairment of endothelial function precedes and exacerbates atherosclerosis. Accordingly, the aim of this study was to investigate a possible link among endothelial dysfunction, subclinical atherosclerosis, and insulin resistance syndrome. First, to examine the association between functional changes of large artery and insulin resistance syndrome, flow-mediated vasodilation (FMD) of the brachial artery was examined by high resolution ultrasonography, as a non-invasive measure of endothelial function in subjects without cardiovascular diseases (n=75). Coronary risk factors, including factors constituting insulin resistance syndrome were evaluated as well. Univariate and multivariate analyses revealed that FMD was inversely correlated with body mass index (BMI; r=-.26, p<0.03), mean arterial pressure (r=-.27, p<0.03), HbA1C (r=-.39, p<0.01), triglyceride (r=-.37, p<0.01), and the number of risk factors (r=-.47, p<0.001). Second, to examine the association between structural changes of large artery and insulin resistance syndrome in apparently healthy subjects (n=545), duplex scanning of the carotid arteries was performed to measure the intima-media thickness (IMT), an index of subclinical atherosclerosis. Age-adjusted-IMT was positively correlated with BMI (r=.14, p<0.002), mean arterial pressure (r=.27, p<0.001), HbA1C (r=.40, p<0.001), triglyceride (r=.12, p<0.005), HOMA, an index of insulin resistance, (r=.17, p<0.007), and the number of risk factors (r=.37, p<0.001). Finally, FMD was inversely correlated with IMT (r=-.28, p<0.03). Thus, the factors constituting insulin resistant syndrome were closely associated with both functional and structural changes of arteries in apparently healthy subjects. Our results suggest that insulin resistance may play a key role in the early process of atherosclerosis.

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.

scholarly journals Repeated Glucose Spikes and Insulin Resistance Synergistically Increase Endothelial Function Vulnerability to High Glucose Levels through Redox Imbalance, and Bardoxolone Methyl (CDDO-Me) Ameliorates Endothelial Dysfunction

2021 ◽  
Author(s):  
Kazuma Ogiso ◽  
Sigfrid Casmir Shayo ◽  
Shigeru Kawade ◽  
Hiroshi Hashiguchi ◽  
Takahisa Deguchi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
High Glucose ◽  
Related Factor ◽  
Redox Imbalance ◽  
Glucose Levels ◽  
Antioxidant Agents

Abstract BackgroundGlucose spikes (GSs) observed after a meal in metabolic syndrome have been reported to cause endothelial dysfunction. However, other insulin resistance-related factors can affect GS-induced endothelial dysfunction. To eliminate these confounding factors, we investigated the separate and combined effects of GSs and insulin resistance due to diet-induced obesity on endothelial function and clarified whether bardoxolone methyl (CDDO-Me), a novel nuclear factor erythroid 2-related factor 2 (Nrf2) activator, protects against GS-induced endothelial dysfunction.MethodsIn the first cohort, eight-week-old male Wistar rats were assigned to one of four groups: 1) control diet (CD)-GS (-); 2) CD-GS (+); 3) Western-type diet (WTD)-GS (-); and 4) WTD-GS (+). Rats were fed a CD or WTD for 13 weeks and intraperitoneally injected with saline or glucose for 1 week twice daily at 20 weeks of age. In the second cohort, four groups from the first cohort were additionally divided into vehicle and CDDO-Me (3 mg/kg) groups. At 21 weeks of age, endothelial function was evaluated using isolated thoracic aortas under normal (5.5 mM) and high-glucose (20 mM) conditions. Gene expression was analyzed, and superoxide anion was evaluated by dihydroethidium (DHE) staining of aortas.ResultsIn the first cohort, endothelium-dependent relaxation (EDR) in the CD-GS (+) or WTD-GS (-) group was comparable to that in the CD-GS (-) group, but it deteriorated in the WTD-GS (+) group only under high-glucose conditions. Antioxidant agents, such as superoxide dismutase, catalase, apocynin (a NOX inhibitor) and Mito-TEMPO (a mitochondrial-targeted superoxide scavenger), improved endothelial function. In this group, upregulation of NOX2 expression and downregulation of SOD2 and catalase expression were observed in the aortas, and DHE intensity was enhanced. In the second cohort, pretreatment of the WTD-GS (+) group with CDDO-Me attenuated this endothelial dysfunction accompanied by a correction of redox imbalance in gene expression and an attenuation of DHE intensity.ConclusionWe demonstrated that GSs and insulin resistance synergistically increased endothelial function vulnerability to high-glucose levels through redox imbalance, although each factor alone had little effect on endothelial function. Furthermore, we showed that pretreatment with CDDO-Me ameliorated endothelial dysfunction caused by GSs in metabolic syndrome model rats.

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