scholarly journals Obesity and asthma: co-morbidity or causal relationship?

2016 ◽  
Vol 73 (3) ◽  
Author(s):  
A. Van Huisstede ◽  
G.J. Braunstahl
Keyword(s):  
Metabolic Syndrome ◽  
Systemic Inflammation ◽  
Low Grade ◽  
Fat Tissue ◽  
Rigorous Approach ◽  
The Metabolic Syndrome ◽  
Bronchial Inflammation ◽  
Co Morbidity ◽  
Few Data ◽  
The Relationship

There is substantial evidence that obesity and asthma are related. “Obese asthma” may be a unique phenotype of asthma, characterized by decreased lung volumes, greater symptoms for a given degree of lung function impairment, destabilization or lack of asthma control, lack of eosinophilic inflammation and a different response to controller medication. Whether this relationship between obesity and asthma is causal or represents co-morbidity due to other factors is unclear. In previous reviews concerning the relationship between obesity and asthma, five hypotheses were put forth. One of these hypotheses is that a low grade systemic inflammation caused by adipokines from the fat tissue causes or enhances bronchial inflammation. In animal models, there is an increasing amount of evidence for the role of adipokines derived from fat tissue in the relationship between obesity and asthma. The data are conflicting in humans. Since obesity is a component of the metabolic syndrome and the metabolic syndrome is also a form of systemic inflammation, it is to be expected that there is a relationship between metabolic syndrome and asthma. The few data that are available show that there is no relationship between metabolic syndrome and asthma, but there is one between the metabolic syndrome and asthma-like symptoms. Further research is needed to confirm the relationship between obesity and asthma in humans, where a rigorous approach in the diagnosis of asthma is essential.

scholarly journals Systemic Inflammation in Metabolic Syndrome: Increased Platelet and Leukocyte Activation, and Key Role of CX3CL1/CX3CR1 and CCL2/CCR2 Axes in Arterial Platelet-Proinflammatory Monocyte Adhesion

2019 ◽  
Vol 8 (5) ◽  
pp. 708 ◽  
Author(s):  
Patrice Marques ◽  
Aida Collado ◽  
Sergio Martinez-Hervás ◽  
Elena Domingo ◽  
Esther Benito ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Systemic Inflammation ◽  
Immune Cell ◽  
Flow Chamber ◽  
Low Grade ◽  
Monocyte Adhesion ◽  
The Metabolic Syndrome ◽  
Factor Α ◽  
Arterial Endothelium

Background: Metabolic syndrome is associated with low-grade systemic inflammation, which is a key driver of premature atherosclerosis. We characterized immune cell behavior in metabolic syndrome, its consequences, and the potential involvement of the CX3CL1/CX3CR1 and CCL2/CCR2 chemokine axes. Methods: Whole blood from 18 patients with metabolic syndrome and 21 age-matched controls was analyzed by flow cytometry to determine the leukocyte immunophenotypes, activation, platelet-leukocyte aggregates, and CX3CR1 expression. ELISA determined the plasma marker levels. Platelet-leukocyte aggregates adhesion to tumor necrosis factor-α (TNFα)-stimulated arterial endothelium and the role of CX3CL1/CX3CR1 and CCL2/CCR2 axes was investigated with the parallel-plate flow chamber. Results: When compared with the controls, the metabolic syndrome patients presented greater percentages of eosinophils, CD3+ T lymphocytes, Mon2/Mon3 monocytes, platelet-eosinophil and -lymphocyte aggregates, activated platelets, neutrophils, eosinophils, monocytes, and CD8+ T cells, but lower percentages of Mon1 monocytes. Patients had increased circulating interleukin-8 (IL-8) and TNFα levels and decreased IL-4. CX3CR1 up-regulation in platelet-Mon1 monocyte aggregates in metabolic syndrome patients led to increased CX3CR1/CCR2-dependent platelet-Mon1 monocyte adhesion to dysfunctional arterial endothelium. Conclusion: We provide evidence of generalized immune activation in metabolic syndrome. Additionally, CX3CL1/CX3CR1 or CCL2/CCR2 axes are potential candidates for therapeutic intervention in cardiovascular disorders in metabolic syndrome patients, as their blockade impairs the augmented arterial platelet-Mon1 monocyte aggregate adhesiveness, which is a key event in atherogenesis.

scholarly journals Problems of Pathogenesis and Pathogenetic Therapy of COVID-19 from the Perspective of the General Theory of Pathological Systems (General Pathological Processes)

2021 ◽  
Vol 22 (14) ◽  
pp. 7582
Author(s):  
Evgenii Gusev ◽  
Alexey Sarapultsev ◽  
Desheng Hu ◽  
Valeriy Chereshnev
Keyword(s):  
Systemic Inflammation ◽  
Pathological Process ◽  
The State ◽  
The Other ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
The Metabolic Syndrome ◽  
Other Hand ◽  
Pathogenetic Therapy ◽  
Fundamental Medicine

The COVID-19 pandemic examines not only the state of actual health care but also the state of fundamental medicine in various countries. Pro-inflammatory processes extend far beyond the classical concepts of inflammation. They manifest themselves in a variety of ways, beginning with extreme physiology, then allostasis at low-grade inflammation, and finally the shockogenic phenomenon of “inflammatory systemic microcirculation”. The pathogenetic core of critical situations, including COVID-19, is this phenomenon. Microcirculatory abnormalities, on the other hand, lie at the heart of a specific type of general pathological process known as systemic inflammation (SI). Systemic inflammatory response, cytokine release, cytokine storm, and thrombo-inflammatory syndrome are all terms that refer to different aspects of SI. As a result, the metabolic syndrome model does not adequately reflect the pathophysiology of persistent low-grade systemic inflammation (ChSLGI). Diseases associated with ChSLGI, on the other hand, are risk factors for a severe COVID-19 course. The review examines the role of hypoxia, metabolic dysfunction, scavenger receptors, and pattern-recognition receptors, as well as the processes of the hemophagocytic syndrome, in the systemic alteration and development of SI in COVID-19.

Metabolic activity of visceral fat and immune-related organs evaluated by 18F-FDG PET/CT is associated with the metabolic syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Pahk ◽  
H.W Kwon ◽  
J.S Eo ◽  
H.S Seo ◽  
S Kim
Keyword(s):  
Metabolic Syndrome ◽  
Systemic Inflammation ◽  
Metabolic Activity ◽  
Fdg Pet ◽  
Inflammatory Activity ◽  
The Metabolic Syndrome ◽  
Inflammatory Status ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct

Abstract Background The risk of cardiovascular disease (CVD) is elevated in metabolic syndrome (MS) and is related to the inflammatory activity of visceral adipose tissue (VAT). We investigated whether the metabolic activity in VAT, assessed by 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT), is associated with systemic inflammatory status, and related to the number of MS components. Methods 18F-FDG PET/CT was performed in a total of 203 subjects: 59 without an MS component; M(0), 92 with one or two MS components; M(1–2), and 52 with MS. Metabolic activity of VAT was evaluated using the mean standardized uptake value (SUVmean) and the maximum SUV (SUVmax). Metabolic activities of immune-related organs such as spleen and bone marrow (BM) were evaluated using the SUVmax. Results VAT SUVmax correlated with high-sensitivity C-reactive protein (hsCRP) and the SUVmax of spleen and BM, which reflect the status of systemic inflammation. Both hsCRP and the SUVmax of the spleen and BM were higher in the MS group than in the M(1–2) or M(0) groups. In VAT, SUVmax increased with increasing number of MS components, while SUVmean decreased. Conclusions The SUVmax of VAT assessed by 18F-FDG PET/CT could reflect the inflammatory activity of VAT which is increased in the MS patients with systemic inflammation. Funding Acknowledgement Type of funding source: None

scholarly journals Serum IGF1, metabolic syndrome, and incident cardiovascular disease in older people: a population-based study

2013 ◽  
Vol 168 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Christa C van Bunderen ◽  
Mirjam M Oosterwerff ◽  
Natasja M van Schoor ◽  
Dorly J H Deeg ◽  
Paul Lips ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Older People ◽  
Population Based ◽  
Mortality Data ◽  
The Metabolic Syndrome ◽  
Longitudinal Aging Study Amsterdam ◽  
Aging Study ◽  
Definition Of ◽  
Relationship Of ◽  
The Relationship

ObjectiveHigh as well as low levels of IGF1 have been associated with cardiovascular diseases (CVD). The relationship of IGF1 with (components of) the metabolic syndrome could help to clarify this controversy. The aims of this study were: i) to investigate the association of IGF1 concentration with prevalent (components of) the metabolic syndrome; and ii) to examine the role of (components of) the metabolic syndrome in the relationship between IGF1 and incident CVD during 11 years of follow-up.MethodsData were used from the Longitudinal Aging Study Amsterdam, a cohort study in a representative sample of the Dutch older population (≥65 years). Data were available in 1258 subjects. Metabolic syndrome was determined using the definition of the US National Cholesterol Education Program Adult Treatment Panel III. CVD were ascertained by self-reports and mortality data.ResultsLevels of IGF1 in the fourth quintile were associated with prevalent metabolic syndrome compared with the lowest quintile (odds ratio: 1.59, 95% confidence interval (CI) 1.09–2.33). The middle up to the highest quintile of IGF1 was positively associated with high triglycerides in women. Metabolic syndrome was not a mediator in the U-shaped relationship of IGF1 with CVD. Both subjects without the metabolic syndrome and low IGF1 levels (hazard ratio (HR) 1.75, 95% CI 1.12–2.71) and subjects with the metabolic syndrome and high IGF1 levels (HR 2.28, 95% CI 1.21–4.28) demonstrated increased risks of CVD.ConclusionsIn older people, high-normal IGF1 levels are associated with prevalent metabolic syndrome and high triglycerides. Furthermore, this study suggests the presence of different pathomechanisms for both low and high IGF1 levels and incident CVD.

Abstract P033: Relationship Between Adiponectin Level and Metabolic Syndrome after Weight Loss in Patients with Abdominal Obesity

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Aelita Berezina ◽  
Olga Belyaeva ◽  
Olga Berkovich ◽  
Elena Baranova ◽  
Tatyina Karonova
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Abdominal Obesity ◽  
Metabolic Disorders ◽  
Intervention Program ◽  
Adiponectin Level ◽  
The Metabolic Syndrome ◽  
Outpatient Intervention ◽  
Before And After ◽  
The Relationship

Objective: to investigate the relationship between adiponectin level and metabolic syndrome (MS) after weight loss in patients with abdominal obesity (AO). Method: A 3-year randomized lifestyle intervention trial performed in 153 patients with AO, age 43,2±0,8 yrs, BMI 32,1±1,9 kg/m 2 . 74 patients keep hypocaloric diet (gr.1), 79 patients keep diet and performed aerobic exercise (gr.2). Adiponectin concentration, body mass (BM), waist circumference (WC), body fat (BF), BMI, the levels of BP, glucose, insulin, HOMA-IR, TC, HDL-C, LDL-C, TG, CRP were measured before and after a 3-years outpatient intervention program. Results. 100% patients with AO had some metabolic disorders and 38% had MS before the treatment. The adiponectin levels and others parameters didn’t differ between the groups before intervention (p>0,05). In 3 years 53 (71,6%) and 58 (73,4%) patients from 1 and 2 groups reduced weight. The rate of improving BM, BMI, BF, WC, HDL-C, TG and insulin was grater in patients gr.2 (p<0,05). The favorable dynamics of MS (MS didn’t appeared at the end of study or didn’t registered in patients who had it before) didn’t differ between the groups 1 and 2 (81,1% and 91,4%, p>0,05). The increasing of adiponectin level occurred more often in patients gr.2, than gr.1 (93,1% and 58,5%, p=0,001, respectively). Adiponectin level increased only in patients gr.2 (18,0±1,1mcg/ml and 23,8±1,3 mcg/ml, p= [[Unable to Display Character: &#1088;]]=0,0001), didn’t changed in gr.1 (p>0,05). It was established that in patients with combination of weight loss and increasing of adiponectin level favorable dynamics of MS occurred more often than in patients who lost weight without increasing of adiponectin level (91,7% and 69,2%, p=0,0001). In patients with favorable dynamics of MS increasing of adiponectin level had met more often, than in patients with unfavorable dynamics of MS (MS continued or appeared) (88,6% and 11,4%, p=0,0001). Increasing of adiponectin level associated with positive dynamics of the MS - OR=9,1 (4,0-20,6). Conclusion. Combination of weight loss and increasing of adiponectin level associated with favorable dynamics of the metabolic syndrome.

The Relationship Between Objectively Measured Physical Activity, Salivary Cortisol, and the Metabolic Syndrome Score in Girls

2014 ◽  
Vol 26 (3) ◽  
pp. 221-230 ◽  
Author(s):  
Katrina D. DuBose ◽  
Andrew J. McKune
Keyword(s):  
Physical Activity ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Waist Circumference ◽  
Body Fat ◽  
Salivary Cortisol ◽  
Sexual Maturity ◽  
Vigorous Physical Activity ◽  
The Metabolic Syndrome ◽  
The Relationship

The relationship between physical activity levels, salivary cortisol, and the metabolic syndrome (MetSyn) score was examined. Twenty-three girls (8.4 ± 0.9 years) had a fasting blood draw, waist circumference and blood pressure measured, and wore an ActiGraph accelerometer for 5 days. Saliva samples were collected to measure cortisol levels. Previously established cut points estimated the minutes spent in moderate, vigorous, and moderate-to-vigorous physical activity. A continuous MetSyn score was created from blood pressure, waist circumference, high-density-lipoprotein (HDL), triglyceride, and glucose values. Correlation analyses examined associations between physical activity, cortisol, the MetSyn score, and its related components. Regression analysis examined the relationship between cortisol, the MetSyn score, and its related components adjusting for physical activity, percent body fat, and sexual maturity. Vigorous physical activity was positively related with 30 min post waking cortisol values. The MetSyn score was not related with cortisol values after controlling for confounders. In contrast, HDL was negatively related with 30 min post waking cortisol. Triglyceride was positively related with 30 min post waking cortisol and area under the curve. The MetSyn score and many of its components were not related to cortisol salivary levels even after adjusting for physical activity, body fat percentage, and sexual maturity.

scholarly journals Systemic, but not local, low-grade endotoxinemia increases plasma sCD163 independently of the cortisol response

2019 ◽  
Vol 8 (2) ◽  
pp. 95-99
Author(s):  
Ermina Bach ◽  
Niels Møller ◽  
Jens Otto L Jørgensen ◽  
Mads Buhl ◽  
Holger Jon Møller
Keyword(s):  
Metabolic Syndrome ◽  
Low Dose ◽  
Human Subjects ◽  
Femoral Vein ◽  
Independent Effect ◽  
Low Grade ◽  
Similar Response ◽  
Dependent Manner ◽  
The Metabolic Syndrome ◽  
And Gender

Aims/hypothesis The macrophage-specific glycoprotein sCD163 has emerged as a biomarker of low-grade inflammation in the metabolic syndrome and related disorders. High sCD163 levels are seen in acute sepsis as a result of direct lipopolysaccharide-mediated shedding of the protein from macrophage surfaces including Kupffer cells. The aim of this study was to investigate if low-grade endotoxinemia in human subjects results in increasing levels of sCD163 in a cortisol-dependent manner. Methods We studied eight male hypopituitary patients and eight age- and gender-matched healthy controls during intravenous low-dose LPS or placebo infusion administered continuously over 360 min. Furthermore, we studied eight healthy volunteers with bilateral femoral vein and artery catheters during a 360-min infusion with saline and low-dose LPS in each leg respectively. Results: Systemic low-grade endotoxinemia resulted in a gradual increase in sCD163 from 1.65 ± 0.51 mg/L (placebo) to 1.92 ± 0.46 mg/L (LPS) at 220 min, P = 0.005 and from 1.66 ± 0.42 mg/L (placebo) to 2.19 ± 0.56 mg/L (LPS) at 340 min, P = 0.006. A very similar response was observed in hypopituitary patients: from 1.59 ± 0.53 mg/L (placebo) to 1.83 ± 0.45 mg/L (LPS) at 220 min, P = 0.021 and from 1.52 ± 0.53 mg/L (placebo) to 2.03 ± 0.44 mg/L (LPS) at 340 min, P < 0.001. As opposed to systemic treatment, continuous femoral artery infusion did not result in increased sCD163. Conclusion: Systemic low-grade endotoxinemia resulted in increased sCD163 to levels seen in the metabolic syndrome in both controls and hypopituitary patients. This suggests a direct and cortisol-independent effect of LPS on the shedding of sCD163. We observed no effect of local endotoxinemia on levels of serum sCD163.

The relationship between the metabolic syndrome defined by various criteria and the extent of coronary artery disease

2008 ◽  
Vol 197 (2) ◽  
pp. 944-950 ◽  
Author(s):  
Takatoshi Kasai ◽  
Katsumi Miyauchi ◽  
Naozumi Kubota ◽  
Hiroshi Tamura ◽  
Takahiko Kojima ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
The Metabolic Syndrome ◽  
Artery Disease ◽  
The Relationship
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