Increased levels and adipose tissue expression of visfatin in morbidly obese women: the relationship with pro-inflammatory cytokines

2012 ◽  
Vol 77 (5) ◽  
pp. 691-698 ◽  
Author(s):  
Ximena Terra ◽  
Teresa Auguet ◽  
Isabel Quesada ◽  
Carmen Aguilar ◽  
Anna Maria Luna ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
Tissue Expression ◽  
Morbidly Obese ◽  
Obese Women ◽  
The Relationship ◽  
Pro Inflammatory Cytokines

scholarly journals Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation

2021 ◽  
Vol 10 (2) ◽  
pp. 169
Author(s):  
Marina Bantulà ◽  
Jordi Roca-Ferrer ◽  
Ebymar Arismendi ◽  
César Picado
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
Inflammatory Process ◽  
Late Onset ◽  
Asthma Risk ◽  
Asthma In Children ◽  
Regulatory Effects ◽  
Developed World ◽  
The Relationship ◽  
Pro Inflammatory Cytokines

Asthma and obesity are two epidemics affecting the developed world. The relationship between obesity and both asthma and severe asthma appears to be weight-dependent, causal, partly genetic, and probably bidirectional. There are two distinct phenotypes: 1. Allergic asthma in children with obesity, which worsens a pre-existing asthma, and 2. An often non allergic, late-onset asthma developing as a consequence of obesity. In obesity, infiltration of adipose tissue by macrophages M1, together with an increased expression of multiple mediators that amplify and propagate inflammation, is considered as the culprit of obesity-related inflammation. Adipose tissue is an important source of adipokines, such as pro-inflammatory leptin, produced in excess in obesity, and adiponectin with anti-inflammatory effects with reduced synthesis. The inflammatory process also involves the synthesis of pro-inflammatory cytokines such as IL-1β, IL-6, TNFα, and TGFβ, which also contribute to asthma pathogenesis. In contrast, asthma pro-inflammatory cytokines such as IL-4, IL-5, IL-13, and IL-33 contribute to maintain the lean state. The resulting regulatory effects of the immunomodulatory pathways underlying both diseases have been hypothesized to be one of the mechanisms by which obesity increases asthma risk and severity. Reduction of weight by diet, exercise, or bariatric surgery reduces inflammatory activity and improves asthma and lung function.

scholarly journals Attenuation of Inflammation and Leptin Resistance by Pyrogallol-Phloroglucinol-6,6-Bieckol on in the Brain of Obese Animal Models

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2773 ◽  
Author(s):  
Myeongjoo Son ◽  
Seyeon Oh ◽  
Junwon Choi ◽  
Ji Tae Jang ◽  
Chang Hu Choi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
Brain Inflammation ◽  
Leptin Resistance ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity ◽  
M1 Polarization ◽  
Activated Macrophage ◽  
The Brain ◽  
Pro Inflammatory Cytokines

Obesity induces inflammation both in the adipose tissue and the brain. Activated macrophage infiltration, polarization of macrophages to a more inflammatory type (M1), and increased levels of pro-inflammatory cytokines are related to brain inflammation, which induces leptin resistance in the brain. Pyrogallol-phloroglucinol-6,6-bieckol (PPB), a compound from Ecklonia cava, has anti-inflammatory effects. In this study, we evaluated the effects of PPB effect M1 polarization and inflammation and its ability to restore the effects of leptin, such as a decrease in appetite and body weight. We administered PPB to diet-induced obesity (DIO) and leptin-deficient (ob/ob) mice, evaluated macrophage activation, polarization, and changes of inflammatory cytokine level in adipose tissue and brain, and determined the effect of PPB on leptin resistance or leptin sensitivity in the brain. The levels of activated macrophage marker, M1/M2, and pro-inflammatory cytokines were increased in the adipose tissue and brain of DIO and ob/ob mice than control. TLR4 expression, endoplasmic reticulum (ER) stress, and NF-κB expression in the brain of DIO and ob/ob mice were also increased; this increase was related to the upregulation of SOCS3 and decreased phosphorylated STAT3, which decreased leptin sensitivity in the brain. PPB decreased inflammation in the brain, restored leptin sensitivity, and decreased food intake and weight gain in both DIO and ob/ob mice.

Is the anti-inflammatory effect of regular exercise responsible for reduced cardiovascular disease?

2007 ◽  
Vol 112 (11) ◽  
pp. 543-555 ◽  
Author(s):  
Kenneth R. Wilund
Keyword(s):  
Cardiovascular Disease ◽  
Inflammatory Cytokines ◽  
Acute Exercise ◽  
Vascular Wall ◽  
Chronic Exercise ◽  
Anti Inflammatory ◽  
The Relationship ◽  
Circulating Levels ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Engaging in regular physical activity reduces the risk of developing CVD (cardiovascular disease), but it is not certain to what degree this may be due to the anti-inflammatory effects of exercise. Following acute exercise, there is a transient increase in circulating levels of anti-inflammatory cytokines, whereas chronic exercise reduces basal levels of pro-inflammatory cytokines. Exercise training also induces the expression of antioxidant and anti-inflammatory mediators in the vascular wall that may directly inhibit the development of atherosclerosis. Limited studies in humans and more comprehensive assessments in animal models have confirmed that exercise is atheroprotective and helped identify a number of the mechanisms to explain these effects. This review explores the relationship between systemic and vascular wall inflammation and the role that the anti-inflammatory effects of exercise have on the development and progression of CVD.

The relationship between oral mucositis and levels of pro-inflammatory cytokines in serum and in gingival crevicular fluid in allogeneic stem cell recipients

2014 ◽  
Vol 23 (6) ◽  
pp. 1749-1757 ◽  
Author(s):  
Karin Garming Legert ◽  
Georgios Tsilingaridis ◽  
Mats Remberger ◽  
Olle Ringdèn ◽  
Anders Heimdahl ◽  
...  
Keyword(s):  
Stem Cell ◽  
Inflammatory Cytokines ◽  
Oral Mucositis ◽  
Gingival Crevicular Fluid ◽  
Crevicular Fluid ◽  
The Relationship ◽  
Pro Inflammatory Cytokines

scholarly journals Exenatide mitigates inflammation and hypoxia along with improved angiogenesis in obese fat tissue

2019 ◽  
Vol 242 (2) ◽  
pp. 79-89 ◽  
Author(s):  
Yingxin Xian ◽  
Zonglan Chen ◽  
Hongrong Deng ◽  
Mengyin Cai ◽  
Hua Liang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
Receptor Agonist ◽  
Capillary Density ◽  
Angiogenic Factors ◽  
Chow Diet ◽  
Fat Tissue ◽  
Protein Levels ◽  
Glucagon Like Peptide 1 ◽  
Pro Inflammatory Cytokines

Obesity-associated chronic inflammation in adipose tissue is partly attributed to hypoxia with insufficient microcirculation. Previous studies have shown that exenatide, a glucagon-like peptide 1 (GLP-1) receptor agonist, plays an anti-inflammatory role. Here, we investigate its effects on inflammation, hypoxia and microcirculation in white adipose tissue of diet-induced obese (DIO) mice. DIO mice were injected intraperitoneally with exenatide or normal saline for 4 weeks, while mice on chow diet were used as normal controls. The mRNA and protein levels of pro-inflammatory cytokines, hypoxia-induced genes and angiogenic factors were detected. Capillary density was measured by laser confocal microscopy and immunochemistry staining. After 4-week exenatide administration, the dramatically elevated pro-inflammatory cytokines in serum and adipose tissue and macrophage infiltration in adipose tissue of DIO mice were significantly reduced. Exenatide also ameliorated expressions of hypoxia-related genes in obese fat tissue. Protein levels of endothelial markers and pro-angiogenic factors including vascular endothelial growth factor and its receptor 2 were augmented in accordance with increased capillary density by exenatide in DIO mice. Our results indicate that inflammation and hypoxia in adipose tissue can be mitigated by GLP-1 receptor agonist potentially via improved angiogenesis and microcirculation in obesity.

scholarly journals COVID-19 and Obesity: Role of Ectopic Visceral and Epicardial Adipose Tissues in Myocardial Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Adèle Lasbleiz ◽  
Bénédicte Gaborit ◽  
Astrid Soghomonian ◽  
Axel Bartoli ◽  
Patricia Ancel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Intensive Care ◽  
Inflammatory Cytokines ◽  
Visceral Adipose Tissue ◽  
Cardiovascular Events ◽  
Low Grade ◽  
Viral Spread ◽  
Visceral Adipose ◽  
Pro Inflammatory Cytokines

In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 via angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the “cytokine storm” and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.

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