scholarly journals Serum insulin levels are associated with vulnerable plaque components in the carotid artery: the Rotterdam Study

2020 ◽  
Vol 182 (3) ◽  
pp. 343-350
Author(s):  
Blerim Mujaj ◽  
Daniel Bos ◽  
Maryam Kavousi ◽  
Aad van der Lugt ◽  
Jan A Staessen ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Carotid Atherosclerosis ◽  
Serum Insulin ◽  
Intraplaque Hemorrhage ◽  
Rotterdam Study ◽  
Lipid Core ◽  
Insulin Levels ◽  
Glucose Levels

Background To investigate the association between fasting serum insulin and glucose levels with atherosclerotic plaque composition in the carotid artery. Impaired insulin and glucose levels are implicated in the etiology of cardiovascular disease; however, their influence on the formation and composition of atherosclerotic plaque remains unclear. Methods In 1740 participants (mean age 72.9 years, 46% women, 14.4% diabetes mellitus) from the population-based Rotterdam Study, we performed carotid MRI to evaluate the presence of calcification, lipid core, and intraplaque hemorrhage in carotid atherosclerosis. All participants also underwent blood sampling to obtain information on serum insulin and glucose levels. Using logistic regression models, we assessed the association of serum insulin and glucose levels (per s.d. and in tertiles) with the different plaque components, while adjusting for sex, age, intima-media thickness, and cardiovascular risk factors. Results Serum insulin levels were associated with the presence of intraplaque hemorrhage (adjusted odds ratio (OR): 1.42 (95% CI: 1.12–1.7)) We found no association with the presence of calcification or lipid core. Sensitivity analyses restricted to individuals without diabetes mellitus yielded similar results. No associations were found between serum glucose levels and any of the plaque components. Conclusions Serum insulin levels are associated with the presence of vulnerable components of carotid plaque, specifically with intraplaque hemorrhage. These findings suggest a complex role for serum insulin in the pathophysiology of carotid atherosclerosis and in plaque vulnerability.

scholarly journals Serum Insulin Levels Are Associated With Plaque Composition In The Carotid Artery: The Rotterdam Study

2019 ◽  
Vol 287 ◽  
pp. e53
Author(s):  
B. Mujaj ◽  
D. Bos ◽  
M. Vernooij ◽  
A. van der Lugt ◽  
T. Muka ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Serum Insulin ◽  
Rotterdam Study ◽  
Plaque Composition ◽  
Insulin Levels

scholarly journals Coexistence of Calcification, Intraplaque Hemorrhage and Lipid Core within the Asymptomatic Atherosclerotic Carotid Plaque: The Rotterdam Study

2015 ◽  
Vol 39 (5-6) ◽  
pp. 319-324 ◽  
Author(s):  
Quirijn J.A. van den Bouwhuijsen ◽  
Daniel Bos ◽  
M. Arfan Ikram ◽  
Albert Hofman ◽  
Gabriel P. Krestin ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Carotid Plaque ◽  
Population Based ◽  
Intraplaque Hemorrhage ◽  
Wall Thickening ◽  
Lower Prevalence ◽  
Rotterdam Study ◽  
Lipid Core ◽  
Logistic Regression Models ◽  
The Relationship

Background: There is a growing amount of evidence suggesting that the composition of carotid atherosclerotic plaques may be of clinical relevance. Yet, little is known on the coexistence of potentially vulnerable and stabilizing components within asymptomatic plaques. Therefore, in this study we set out to investigate the coexistence of intraplaque calcification, hemorrhage and lipid core within the carotid artery using a multi-modality imaging approach. Methods: In 329 subjects from the population-based Rotterdam Study, all with ultrasound-confirmed carotid wall thickening, we performed a multi-detector CT and a high-resolution MRI of the carotid artery bifurcation at both sides. On the CT examinations, we quantified the volume of intraplaque calcification, and using the MRI examinations we rated the presence of intraplaque hemorrhage and of lipid core. In total, we investigated 611 carotid arteries with plaques. With logistic regression models we investigated the relationship of calcification volume - as a potential stabilizing component - with the presence of potential vulnerable components (intraplaque hemorrhage and lipid core) within each carotid plaque. We adjusted all analyses for age, sex and maximal plaque thickness. Next, we stratified on degree of stenosis (≤ or >30%) to evaluate effect modification by atherosclerotic burden. Results: We found that a larger calcification volume was associated with a higher prevalence of intraplaque hemorrhage, and a lower prevalence of lipid core (fully-adjusted odds ratio (OR) per standard deviation (SD) increase in calcification volume: 2.04 (95% confidence intervals (CI): 1.49; 2.78) and 0.72 (95% CI: 0.58; 0.90), respectively). Stratification on the degree of stenosis showed no difference in the association between calcification volume and hemorrhage over strata, while the relationship between a larger calcification volume and a lower prevalence of lipid seemed more pronounced in persons with a high degree of stenosis. Conclusions: In this population-based setting, we found that there is a complex relationship between calcification, intraplaque hemorrhage and lipid core within the carotid atherosclerotic plaque. Plaques with a higher load of calcification contain more often hemorrhagic components, but less often lipid core. Our results suggest that both in small and large plaques, intraplaque calcification may not be a stabilizing factor per se. These findings create an urge for conducting prospective studies investigating the interrelation of these different plaque components with regard to future cerebrovascular events.

Abstract 3482: Increased Matrix Metalloproteinase-9 Expression is Correlated with Carotid Intraplaque hemorrhage in a Swine Model

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Zhong-Song Shi ◽  
Xiao-Bing Jiang ◽  
Jin-Shan Wang ◽  
Wei-Si Yuan ◽  
Dong-Hong Liu
Keyword(s):  
Carotid Artery ◽  
Matrix Metalloproteinase ◽  
Vulnerable Plaque ◽  
Carotid Plaque ◽  
Carotid Atherosclerosis ◽  
Intraplaque Hemorrhage ◽  
Swine Model ◽  
Carotid Plaques ◽  
Rete Mirabile ◽  
Atherosclerotic Changes

Purpose: The limited number of large animal carotid atherosclerotic models restricts the preclinical evaluation of endovascular therapies. Carotid intraplaque hemorrhage may be associated with a higher risk of ischemic stroke in patients with carotid disease. In this study, we assess the association of the lesional expression of matrix metalloproteinase (MMP)-9 with vulnerable atherosclerotic carotid plaque and intraplaque hemorrhage in a Swine model. Materials and Methods: Carotid atherosclerosis was induced in miniswines using the combination of partial ligation and high cholesterol diet, and a minimum 70% stenosis was confirmed by Doppler ultrasonography immediately post-ligation. Carotid artery sections were obtained for histopathological examination and immunohistochemical study for MMP-9 at three months. Distal embolism was determined by the presence of atheroemboli in the ipsilateral rete mirabile. Atherosclerotic changes were classified by AHA/Stary stage (type I to VI). The association of distal embolism in the rete mirabile with vulnerable carotid plaque was analyzed. The association of MMP-9 expression in the plaque with the vulnerable plaque and intraplaque hemorrhage was further analyzed. Results: One hundred ninety-one carotid segments from ten carotid artery models were assessed. Among 139 segments with atherosclerotic changes, 102 segments had vulnerable plaque (Stary IV to VI). Vulnerable atherosclerotic plaques were found more frequently in the vessel wall proximal to the partial ligation than distal ( P <0.0001). Distal embolism was found in all 10 rete mirabilis, and deemed to be from the ipsilateral vulnerable carotid plaques. Areas positive for MMP-9 tended to be greater in the vulnerable plaque than in the stable plaque (8.69 ± 0.73% vs. 7.04 ± 0.94%, p=0.35). Areas positive for MMP-9 were significantly greater in the plaque with intraplaque hemorrhage than in the plaque without intraplaque hemorrhage (11.84 ± 1.22% vs. 6.63 ± 0.59%, p<0.001). On multivariate analysis, positive expression of MMP-9 was an independent predictor of intraplaque hemorrhage (p=0.007). Conclusion: Vulnerable carotid plaques with distal embolism were created in a Swine model of carotid atherosclerosis. Increased expression of MMP-9 may be associated with vulnerable carotid plaques, especially having the feature of intraplaque hemorrhage.

Hypothalamic noradrenergic and sympathoadrenal control of glycemia after stress

1989 ◽  
Vol 256 (2) ◽  
pp. E231-E235
Author(s):  
G. A. Smythe ◽  
W. S. Pascoe ◽  
L. H. Storlien
Keyword(s):  
Insulin Release ◽  
Acute Stress ◽  
Serum Insulin ◽  
Elevated Serum ◽  
Serum Glucose ◽  
Neural Pathways ◽  
Swim Stress ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Positive Correlations

Central noradrenergic pathways play a significant role in mediating blood glucose levels after neuroglycopenia. To further investigate hypothalamic noradrenergic neuronal activity (NNA) and sympathoadrenal influences in glucoregulation, we studied the effects of acute stress on glycemia and insulin release in normal and adrenalectomized (ADRX) rats. Within 5 min of exposure of rats to ether or cold-swim stress, significant positive correlations were evident between hypothalamic NNA and serum glucose levels (r = 0.70, P less than 0.001; at 15 min r = 0.78, P less than 0.0001). Five minutes after stress in the intact rat, insulin release was inhibited and serum insulin levels inversely correlated to hypothalamic NNA (r = 0.45, P less than 0.05). This relationship between insulin and NNA was no longer present 15 min after stress, but the levels of insulin remained inappropriately low with respect to the elevated serum glucose levels (approximately 30% above basal). Blockade of sympathetic noradrenergic pathways by treatment of intact rats with guanethidine prevented the rise in glucose after cold-swim stress but did not prevent the inhibition of insulin release. Fifteen minutes after exposure of ADRX rats to cold-swim stress their hypothalamic NNA and serum glucose levels were similar to intact animals. However, in contrast to their intact counterparts, serum insulin levels were significantly elevated (P less than 0.01). These data are consistent with central noradrenergic neural pathways directly mediating hepatic glucose release and indirectly inhibiting pancreatic insulin release via activation of adrenal medullary catecholamines.

scholarly journals Aerobic exercise improves LPS-induced sepsis via regulating the Warburg effect in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xishuai Wang ◽  
Zhiqing Wang ◽  
Donghui Tang
Keyword(s):  
Blood Glucose ◽  
Mrna Expression ◽  
Serum Insulin ◽  
Pulmonary Inflammation ◽  
Aortic Injury ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Blood Glucose Levels

AbstractWe investigated the impact of aerobic exercise (AE) on multiple organ dysfunction syndrome (MODS), aortic injury, pathoglycemia, and death during sepsis. ICR mice were randomized into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Mice were trained with low-intensity for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ morphology and damage. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, and bronchoalveolar lavage fluid (BALF) cell count, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, serum insulin levels, plasma high-mobility group box 1 (HMGB1) levels, glucose transporter 1 (Glut1) and HMGB1, silent information regulator 1 (Sirt-1), and nuclear factor erythroid 2-related factor 2 (Nrf-2) mRNA expression levels in lung tissue. AE improved sepsis-associated multiple organ dysfunction syndrome (MODS), aortic injury, hypoglycemia, and death. AE prominently decreased pulmonary inflammation, pulmonary edema, and modulated redox balance during sepsis. AE prominently decreased neutrophil content in organ. AE prominently downregulated CXCL-1, CXCL-8, IL-6, TNF-α, Glu1, and HMGB1 mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung during sepsis. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels and serum insulin levels during sepsis. A 4-week AE improves sepsis-associated MODS, aortic injury, pathoglycemia, and death. AE impairs LPS-induced lactate and HMGB1 release partly because AE increases serum insulin levels and decreases the levels of Glut1. AE is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.

Forearm Glucose Uptake in Cirrhosis and Its Relationship to Glucose Tolerance

1980 ◽  
Vol 59 (3) ◽  
pp. 191-198 ◽  
Author(s):  
B. A. Leatherdale ◽  
R. A. Chase ◽  
J. Rogers ◽  
K. G. M. M. Alberti ◽  
P. Davies ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Serum Insulin ◽  
Oral Glucose ◽  
Glucose Load ◽  
Peripheral Tissues ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Control Subjects ◽  
Cirrhotic Patients

1. Oral glucose-tolerance tests (100 g) were carried out in six patients with stable well-compensated cryptogenic cirrhosis and in 12 control subjects. 2. In confirmation of previous studies, patients with cirrhosis had high post-glucose serum insulin levels and were glucose intolerant (mean incremental glucose area 954 ± 186 compared with 482 ± 35 mmol 3 h−11−1 in controls; P<0.05) 3. Forearm arteriovenous differences of glucose and forearm blood flows were measured to estimate the proportion of the glucose load metabolized in peripheral tissues. Values in cirrhotic patients and control subjects (5614 ± 1630 compared with 5344 ± 672 μmol of glucose min−11−1 of forearm in 3 h) were similar despite higher glucose levels and sustained high insulin levels in the cirrhotic patients. 4. Peak lactate concentrations after glucose were of similar magnitude in the two groups (0.66 ± 0.12 compared with 0.62 ± 0.75 mmol/l) but in the patients with cirrhosis the peak occurred later and was more sustained. 5. The glucose intolerance of cirrhosis is primarily due to impaired hepatic retention of the glucose load. Insulin resistance in peripheral tissues-5-also be important since the higher insulin concentrations found in cirrhotic patients failed to enhance peripheral glucose uptake.

scholarly journals Analysis of MicroRNAs Associated With Carotid Atherosclerotic Plaque Rupture With Thrombosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Peng Nie ◽  
Fan Yang ◽  
Fang Wan ◽  
Shuxuan Jin ◽  
Jun Pu
Keyword(s):  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Vascular Wall ◽  
Intraplaque Hemorrhage ◽  
Control Group ◽  
Left Carotid Artery ◽  
Mirna Microarray ◽  
Post Surgery ◽  
Atherosclerotic Plaque Rupture

Atherosclerosis is a progressive vascular wall inflammatory disease, and the rupture of atherosclerotic vulnerable plaques is the leading cause of morbidity and mortality worldwide. This study intended to explore the potential mechanisms behind plaque rupture and thrombosis in ApoE knockout mice. The spontaneous plaque rupture models were established, and left carotid artery tissues at different time points (1-, 2-, 4-, 6-, 8-, 12-, and 16-week post-surgery) were collected. By the extent of plaque rupture, plaque was defined as (1) control groups, (2) atherosclerotic plaque group, and (3) plaque rupture group. Macrophage (CD68), MMP-8, and MMP-13 activities were measured by immunofluorescence. Cytokines and inflammatory markers were measured by ELISA. The left carotid artery sample tissue was collected to evaluate the miRNAs expression level by miRNA-microarray. Bioinformatic analyses were conducted at three levels: (2) vs. (1), (3) vs. (2), and again in seven time series analysis. The plaque rupture with thrombus and intraplaque hemorrhage results peaked at 8 weeks and decreased thereafter. Similar trends were seen in the number of plaque macrophages and lipids, the expression of matrix metalloproteinase, and the atherosclerotic and plasma cytokine levels. MiRNA-microarray showed that miR-322-5p and miR-206-3p were specifically upregulated in the atherosclerotic plaque group compared with those in the control group. Meanwhile, miR-466h-5p was specifically upregulated in the plaque rupture group compared with the atherosclerotic plaque group. The highest incidence of plaque rupture and thrombosis occurred at 8 weeks post-surgery. miR-322-5p and miR-206-3p may be associated with the formation of atherosclerotic plaques. miR-466h-5p may promote atherosclerotic plaque rupture via apoptosis-related pathways.

scholarly journals Evaluation of ameliorative effect of sodium nitrate in experimental model of streptozotocin-induced diabetic neuropathy in male rats

2019 ◽  
Vol 53 (1) ◽  
pp. 14-25 ◽  
Author(s):  
Hajar Oghbaei ◽  
Mohammad Reza Alipour ◽  
Gisou Mohaddes ◽  
Gholam Reza Hamidian ◽  
Rana Keyhanmanesh
Keyword(s):  
Serum Insulin ◽  
The Body ◽  
Male Rats ◽  
Diabetes Group ◽  
Insulin Levels ◽  
Nitrate Treatment ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Ameliorative Effect ◽  
Male Wistar Rats

AbstractObjective. Diabetes induces sensory symptoms of neuropathy as positive (hyperalgesia), negative (hypoalgesia), or both.Methods. In the present study, fifty male Wistar rats were allocated to five groups: control, control+nitrate, diabetes, diabetes+insulin, and diabetes+nitrate. Thirty days after diabetes confirmation, insulin (2–4 U/day) was injected subcutaneously in diabetes+insulin group and nitrate (100 mg/l) was added into drinking water of the control+nitrate and diabetes+nitrate groups for a period of 2 months. In order to assess the mechanical and thermal algesia, tail immersion, hot plate, and von Frey tests were performed. The serum insulin levels were determined with insulin ELISA Kit. Serum level of NOx was determined by the Griess method.Results. Both thermal and mechanical nociceptive thresholds showed a significant decrease (p<0.05) which was followed by a significant increase (p<0.01) in the thermal nociceptive threshold in the diabetes group. Chronic nitrate or insulin treatment led to a significant decrease (p<0.01) in blood glucose levels, as well as a significant (p<0.05) increase in the body weight and serum NOx. Moreover, nitrate treatment significantly increased serum insulin levels (p<0.001) compared to the other groups.Conclusion. Chronic nitrate treatment modified the thermal and mechanical sensitivities in diabetic animals.

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