scholarly journals Relation of Endothelial Dysfunction and Adipokines Levels to Insulin Resistance in Metabolic Syndrome Patients

2009 ◽  
Vol 63 (4-5) ◽  
pp. 222-227
Author(s):  
Pēteris Tretjakovs ◽  
Antra Jurka ◽  
Inga Bormane ◽  
Indra Miķelsone ◽  
Dace Reihmane ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Doppler Imaging ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Cytokines And Chemokines ◽  
Tnf Α ◽  
Artery Disease ◽  
D 20

Relation of Endothelial Dysfunction and Adipokines Levels to Insulin Resistance in Metabolic Syndrome Patients Obese metabolic syndrome (MS) patients were categorised into three groups: 44 with type 2 diabetes mellitus (T2DM)(D); 20 with T2DM and coronary artery disease (CAD) (DC), and 26 with MS alone (M). Eighteen healthy subjects were selected as controls (C). Insulin resistance (IR) was assessed by HOMA-IR. Adiponectin, tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and interleukin-8 (IL-8) concentrations were measured by xMAP technology. Endothelin-1 (ET-1) was determined by ELISA. We used laser Doppler imaging for evaluating cutaneous endothelium-dependent vasodilatation in the hand. D and DC groups had significantly elevated IR compared with M or C group (P < 0.01). TNF-α, IL-6, IL-8, MCP-1 and ET-1 levels in DC were significantly elevated compared with other groups (P < 0.001). IL-6, IL-8, MCP-1 and ET-1 in D group were higher than those in C group (P < 0.05). TNF-α, IL-6, IL-8, MCP-1 and ET-1 concentrations were correlated with HOMA-IR indexes and adiponectin levels. All patients had lower adiponectin concentrations than controls (P < 0.001), but there were no differences between the patient groups. Only D and DC groups demonstrated a significant and similar decrease in LDI-Ach marker compared to C group (P < 0.001). LDI-Ach values were significantly correlated with HOMA-IR indexes and adiponectin levels (P < 0.001). Our findings show that obese MS patients have significantly increased HOMA-IR, TNF-α, IL-6, MCP-1 and IL-8 levels, decreased adiponectin concentration, and endothelial dysfunction, but the presence of T2DM and CAD in these patients is associated with more pronounced endothelial dysfunction and increased production of inflammatory cytokines and chemokines.

scholarly journals Relationship between endothelial dysfunction and development of complications of metabolic syndrome

2018 ◽  
Vol 99 (5) ◽  
pp. 784-791
Author(s):  
A G Mustafaeva
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Smooth Muscles ◽  
Circulatory System ◽  
Vascular Wall ◽  
Vascular Walls ◽  
Increased Risk ◽  
Normal Tone ◽  
Almost All

The article presents the analysis of literature data on the pathogenetic role of endothelial dysfunction (ED) in the development of complications of metabolic syndrome (MS). There are two main signs of MS development - abdominal obesity (AO) and primary insulin resistance (IR). IR and concomitant hyperinsulinemia have both direct and indirect atherogenic effects on vascular walls, lead to the development of dyslipidemia, a number of hormonal and metabolic disorders, activation of the sympathoadrenal system, ie, are the basis of almost all components of MS. Despite the high margin of safety of the circulatory system, there comes a time when, due to frequent vasoconstrictor effects thickening of the walls of resistive vessels occurs to limit local perfusion. The thickening of the walls of arteries develops, that is, the modeling of the vascular wall occurs, leading to an increase of the total peripheral vascular resistance with normal tone of smooth muscles. Currently, the concept of ED is formulated as a key link of insulin resistance and atherogenesis in MS. Methods for studying endothelial function have been created and are introduced into clinical practice. New approaches to directed correction of endothelial dysfunction are being developed. Prospective studies have shown that the degree of endothelial dysfunction may be important in predicting cardiovascular events in patients with or without identified vascular disease. Probably, ED may also be related to the pathogenesis of diabetes mellitus type 2 (DM2). Since all components of MS can have an adverse effect on endothelium, ED can be an extremely common phenomenon in patients with metabolic syndrome and can act as a predictor of increased risk of cardiovascular diseases and DM2 in this population.

scholarly journals Enzyme Degradation and Proinflammatory Activity in Arthritogenic and Nonarthritogenic Eubacterium aerofaciens Cell Walls

2001 ◽  
Vol 69 (12) ◽  
pp. 7277-7284 ◽  
Author(s):  
Xiang Zhang ◽  
Marja Rimpiläinen ◽  
Egle Šimelyte ◽  
Paavo Toivanen
Keyword(s):  
Proinflammatory Cytokines ◽  
Chronic Arthritis ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Enzyme Degradation ◽  
Tnf Α ◽  
Stimulatory Capacity ◽  
Normal Human ◽  
Proinflammatory Activity ◽  
Factor Alpha

ABSTRACT Two almost-identical strains of Eubacterium aerofaciens isolated from the normal human gut flora were used. The cell wall (CW) of one strain with a peptidoglycan (PG) type A4α induces chronic arthritis in the rat after a single intraperitoneal injection, whereas CW of the other with PG type A4β induces only a transient acute arthritis. The CW of the arthritogenic E. aerofaciens was a twofold-more-potent stimulator of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) than the nonarthritogenic CW. After degradation with mutanolysin, the capacity of the arthritogenic PG to stimulate production of TNF-α and MCP-1 was significantly increased, whereas that of the nonarthritogenic PG was significantly decreased. In other words, after enzyme degradation the arthritogenic PG had a four- to fivefold-stronger stimulatory capacity than that of the enzyme-treated nonarthritogenic PG. These findings indicate that the arthritogenicity of CW or a PG is not dependent on the enzyme resistance alone but also on how the PG fragments released by enzyme degradation stimulate the production of proinflammatory cytokines.

scholarly journals Mycoplasma pneumoniae-Derived Lipopeptides Induce Acute Inflammatory Responses in the Lungs of Mice

2007 ◽  
Vol 76 (1) ◽  
pp. 270-277 ◽  
Author(s):  
Takashi Shimizu ◽  
Yutaka Kida ◽  
Koichi Kuwano
Keyword(s):  
Mycoplasma Pneumoniae ◽  
Inflammatory Responses ◽  
Lavage Fluid ◽  
Peritoneal Macrophages ◽  
Necrosis Factor Alpha ◽  
Chemokine Production ◽  
Cytokines And Chemokines ◽  
Tnf Α ◽  
Mouse Peritoneal Macrophages

ABSTRACT The pathogenesis of Mycoplasma pneumoniae infection is considered to be in part attributable to excessive immune responses. In this study, we investigated whether synthetic lipopeptides of subunit b of F0F1-type ATPase (F0F1-ATPase), NF-κB-activating lipoprotein 1 (N-ALP1), and N-ALP2 (named FAM20, sN-ALP1, and sN-ALP2, respectively) derived from M. pneumoniae induce cytokine and chemokine production and leukocyte infiltration in vivo. Intranasal administration of FAM20 and sN-ALP2 induced infiltration of leukocyte cells and production of chemokines and cytokines in bronchoalveolar lavage fluid, but sN-ALP1 failed to do so. The activity of FAM20 was notably higher than that of sN-ALP2. FAM20 and sN-ALP2 induced tumor necrosis factor alpha (TNF-α) through Toll-like receptor 2 in mouse peritoneal macrophages. Moreover, in the range of low concentrations of lipopeptides, FAM20 showed relatively high activity of inducing TNF-α in mouse peritoneal macrophages compared to synthetic lipopeptides such as MALP-2 and FSL-1, derived from Mycoplasma fermentans and Mycoplasma salivarium, respectively. These findings indicate that the F0F1-ATPase might be a key molecule in inducing cytokines and chemokines contributing to inflammatory responses during M. pneumoniae infection in vivo.

scholarly journals -308G/A polymorphism of tumor necrosis factor alpha (TNF-α) gene and metabolic syndrome susceptibility: a meta-analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dong Wang ◽  
Liqun He ◽  
Xiaotian Zhang
Keyword(s):  
Metabolic Syndrome ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Dominant Model ◽  
Necrosis Factor Alpha ◽  
Increased Risk ◽  
Tnf Α ◽  
Factor Alpha ◽  
Allele Model ◽  
Necrosis Factor

AbstractMany studies tried to assess the relationship between -308G/A polymorphism of tumor necrosis factor alpha (TNF-α) gene and risk of metabolic syndrome (MS), but their results were contradictory. This meta-analysis aimed to precisely evaluate this association. A systematic literature search was performed in Pubmed database and WanFang Med Online, STATA software 14.0 was used for the meta-analysis. Eleven independent studies containing 3277 cases and 3312 controls were included in our meta-analysis. In overall analysis, significant association was found between -308G/A polymorphism of TNF-α and MS in both allele model (OR 1.47, 95% CI 1.09–1.98, P 0.013) and dominant model (OR 1.77, 95% CI 1.21–2.58, P 0.003). In the subgroup analysis, the A allele was associated with increased risk of MS in Asia group (allele model: OR 1.82 95% CI 1.31–2.53, P < 0.001; dominant model: OR 2.30, 95% CI 1.64–3.21 P < 0.001; homozygous model: OR 2.29, 95% CI 1.31–4.01, P 0.004), and decreased risk of MS in Europe group (dominant model: OR 0.83, 95% CI 0.70–0.99, P < 0.001; recessive model: OR 0.51, 95% CI 0.28–0.92, P 0.025; homozygous model: OR 0.49 95% CI 0.27–0.89, P 0.02). The A allele also appeared to linked to increased risk of MS in CDS group and IDF groups. No significant association was observed in NCEPATPIII group. Our results suggested that -308G/A of TNF-α gene was a risk factor for MS, but it may played different roles in different ethnics, further studies with larger sample size and more other ethnics should be performed to confirm our conclusions.

scholarly journals Potential Biomarkers of Insulin Resistance and Atherosclerosis in Type 2 Diabetes Mellitus Patients with Coronary Artery Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Sharifah Intan Qhadijah Syed Ikmal ◽  
Hasniza Zaman Huri ◽  
Shireene Ratna Vethakkan ◽  
Wan Azman Wan Ahmad
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Coronary Artery Disease ◽  
Type 2 Diabetes Mellitus ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Biological Marker ◽  
Artery Disease

Type 2 diabetes mellitus patients with coronary artery disease have become a major public health concern. The occurrence of insulin resistance accompanied with endothelial dysfunction worsens the state of atherosclerosis in type 2 diabetes mellitus patients. The combination of insulin resistance and endothelial dysfunction leads to coronary artery disease and ischemic heart disease complications. A recognized biological marker, high-sensitivity C-reactive protein, has been used widely to assess the progression of atherosclerosis and inflammation. Along with coronary arterial damage and inflammatory processes, high-sensitivity C-reactive protein is considered as an essential atherosclerosis marker in patients with cardiovascular disease, but not as an insulin resistance marker in type 2 diabetes mellitus patients. A new biological marker that can act as a reliable indicator of both the exact state of insulin resistance and atherosclerosis is required to facilitate optimal health management of diabetic patients. Malfunctioning of insulin mechanism and endothelial dysfunction leads to innate immune activation and released several biological markers into circulation. This review examines potential biological markers, YKL-40, alpha-hydroxybutyrate, soluble CD36, leptin, resistin, interleukin-18, retinol binding protein-4, and chemerin, as they may play significant roles in insulin resistance and atherosclerosis in type 2 diabetes mellitus patients with coronary artery disease.

scholarly journals Involvement of Inflammatory Chemokines in Survival of Human Monocytes Fed with Malarial Pigment

2010 ◽  
Vol 78 (11) ◽  
pp. 4912-4921 ◽  
Author(s):  
Giuliana Giribaldi ◽  
Mauro Prato ◽  
Daniela Ulliers ◽  
Valentina Gallo ◽  
Evelin Schwarzer ◽  
...  
Keyword(s):  
Real Time ◽  
Expression Patterns ◽  
Human Monocytes ◽  
Rt Pcr ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Inflammatory Chemokines ◽  
Factor Alpha

ABSTRACT Hemozoin (HZ)-fed monocytes are exposed to strong oxidative stress, releasing large amounts of peroxidation derivatives with subsequent impairment of numerous functions and overproduction of proinflammatory cytokines. However, the histopathology at autopsy of tissues from patients with severe malaria showed abundant HZ in Kupffer cells and other tissue macrophages, suggesting that functional impairment and cytokine production are not accompanied by cell death. The aim of the present study was to clarify the role of HZ in cell survival, focusing on the qualitative and temporal expression patterns of proinflammatory and antiapoptotic molecules. Immunocytochemical and flow cytometric analyses showed that the long-term viability of human monocytes was unaffected by HZ. Short-term analysis by macroarray of a complete panel of cytokines and real-time reverse transcription (RT)-PCR experiments showed that HZ immediately induced interleukin-1β (IL-1β) gene expression, followed by transcription of eight additional chemokines (IL-8, epithelial cell-derived neutrophil-activating peptide 78 [ENA-78], growth-regulated oncogene α [GROα], GROβ, GROγ, macrophage inflammatory protein 1α [MIP-1α], MIP-1β, and monocyte chemoattractant protein 1 [MCP-1]), two cytokines (tumor necrosis factor alpha [TNF-α] and IL-1receptor antagonist [IL-1RA]), and the cytokine/chemokine-related proteolytic enzyme matrix metalloproteinase 9 (MMP-9). Furthermore, real-time RT-PCR showed that 15-HETE, a potent lipoperoxidation derivative generated by HZ through heme catalysis, recapitulated the effects of HZ on the expression of four of the chemokines. Intermediate-term investigation by Western blotting showed that HZ increased expression of HSP27, a chemokine-related protein with antiapoptotic properties. Taken together, the present data suggest that apoptosis of HZ-fed monocytes is prevented through a cascade involving 15-HETE-mediated upregulation of IL-1β transcription, rapidly sustained by chemokine, TNF-α, MMP-9, and IL-1RA transcription and upregulation of HSP27 protein expression.

scholarly journals Endothelial and inflammatory responses to acute exercise in perimenopausal and late postmenopausal women

2016 ◽  
Vol 311 (5) ◽  
pp. R841-R850 ◽  
Author(s):  
Corinna Serviente ◽  
Lisa M. Troy ◽  
Maxine de Jonge ◽  
Daniel D. Shill ◽  
Nathan T. Jenkins ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Postmenopausal Women ◽  
Acute Exercise ◽  
Inflammatory Responses ◽  
Subclinical Atherosclerosis ◽  
Inflammatory Factors ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tnf Α ◽  
Before And After ◽  
Factor Α

Endothelial dysfunction and inflammation are characteristics of subclinical atherosclerosis and may increase through progressive menopausal stages. Evaluating endothelial responses to acute exercise can reveal underlying dysfunction not apparent in resting conditions. The purpose of this study was to investigate markers of endothelial function and inflammation before and after acute exercise in healthy low-active perimenopausal (PERI) and late postmenopausal (POST) women. Flow-mediated dilation (FMD), CD31+/CD42b− and CD62E+ endothelial microparticles (EMPs), and the circulating inflammatory factors monocyte chemoattractant protein 1 (MCP-1), interleukin 8 (IL-8), and tumor necrosis factor-α (TNF-α) were measured before and 30 min after acute exercise. Before exercise, FMD was not different between groups (PERI: 6.4 ± 0.9% vs. POST: 6.5 ± 0.8%, P = 0.97); however, after acute exercise PERI tended to improve FMD (8.5 ± 0.9%, P = 0.09), whereas POST did not (6.2 ± 0.8%, P = 0.77). Independent of exercise, we observed transient endothelial dysfunction in POST with repeated FMD measures. There was a group × exercise interaction for CD31+/CD42b− EMPs ( P = 0.04), where CD31+/CD42b− EMPs were similar before exercise (PERI: 57.0 ± 6.7 EMPs/μl vs. POST: 58.5 ± 5.3 EMPs/μl, P = 0.86) but were higher in POST following exercise (PERI: 48.2 ± 6.7 EMPs/μl vs. POST: 69.4 ± 5.3 EMPs/μl, P = 0.023). CD62E+ EMPs were lower in PERI compared with POST before exercise ( P < 0.001) and increased in PERI ( P = 0.04) but did not change in POST ( P = 0.68) in response to acute exercise. After acute exercise, MCP-1 ( P = 0.055), TNF-α ( P = 0.02), and IL-8 ( P < 0.001) were lower in PERI but only IL-8 decreased in POST ( P < 0.001). Overall, these data suggest that perimenopausal and late postmenopausal women display different endothelial and inflammatory responses to acute exercise.

scholarly journals Increased Subcutaneous and Epicardial Adipose Tissue Production of Proinflammatory Cytokines in Cardiac Surgery Patients: Possible Role in Postoperative Insulin Resistance

2006 ◽  
Vol 91 (11) ◽  
pp. 4620-4627 ◽  
Author(s):  
Jaromir Kremen ◽  
Marketa Dolinkova ◽  
Jana Krajickova ◽  
Jan Blaha ◽  
Katerina Anderlova ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Cardiac Surgery ◽  
Mrna Expression ◽  
Proinflammatory Cytokines ◽  
Epicardial Adipose Tissue ◽  
Monocyte Chemoattractant Protein 1 ◽  
Elective Cardiac Surgery ◽  
Tnf Α ◽  
History Of

Abstract Context: Hyperglycemia and insulin resistance frequently occur in critically ill patients even without a history of diabetes. Objective: Our objective was to study the role of adipose tissue hormonal production in the development of insulin resistance in cardiac surgery patients. Participants, Interventions, and Settings: Fifteen patients with elective cardiac surgery underwent blood sampling before, at the end, and 6, 12, 24, 48, and 120 h after the end of their operation. Epicardial and sc adipose tissue sampling was done at the beginning and at the end of surgery in the Department of Cardiac Surgery. Main Outcome Measures: We measured serum concentrations and sc and epicardial adipose tissue mRNA expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), TNF-α, leptin, resistin, and adiponectin and sc and epicardial adipose tissue mRNA expression of CD14, CD45, and CD68. Results: The rate of insulin infusion required to maintain euglycemia increased up to 7-fold 12 h after the operation, suggesting the development of insulin resistance. Serum IL-6 levels increased 43-fold 12 h after surgery. MCP-1 peaked 6-fold at the end of surgery. Smaller peaks of TNF-α and leptin appeared 6 and 12 h after surgery, respectively. Resistin levels peaked 4-fold 24 h after surgery, but adiponectin levels were not significantly affected. TNF-α and CD45 mRNA expression increased markedly during the operation in sc adipose tissue. IL-6, resistin, and MCP-1 mRNA expression increased in both sc and epicardial adipose tissue. Leptin, adiponectin, CD14, and CD68 mRNA expression did not change significantly. Conclusions: Both sc and epicardial adipose tissue is a source of proinflammatory cytokines in cardiac surgery patients and may contribute to the development of postoperative insulin resistance.

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