scholarly journals Obesity and lung inflammation

2010 ◽  
Vol 108 (3) ◽  
pp. 722-728 ◽  
Author(s):  
Peter Mancuso
Keyword(s):  
Adipose Tissue ◽  
Lung Disease ◽  
Inflammatory Responses ◽  
Acute Phase Proteins ◽  
Pulmonary Inflammation ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Tissue Mass ◽  
Proinflammatory Mediators ◽  
Increased Risk

The prevalence of obesity has increased dramatically worldwide, predisposing individuals to an increased risk of morbidity and mortality due to cardiovascular disease and type 2 diabetes. Less recognized is the fact that obesity may play a significant role in the pathogenesis of pulmonary diseases through mechanisms that may involve proinflammatory mediators produced in adipose tissue that contribute to a low-grade state of systemic inflammation. In animal models, inflammatory responses in the lung have been shown to influence the production of the adipocytokines, leptin and adiponectin, cytokines, acute phase proteins, and other mediators produced by adipose tissue that may participate in immune responses of the lung. An increased adipose tissue mass may also influence susceptibility to pulmonary infections, enhance pulmonary inflammation associated with environmental exposures, and exacerbate airway obstruction in preexisting lung disease. An increased understanding of the mechanisms by which obesity influences pulmonary inflammation may facilitate the development of novel therapeutic interventions for the treatment of lung disease.

scholarly journals Cellular hypoxia and adipose tissue dysfunction in obesity

2009 ◽  
Vol 68 (4) ◽  
pp. 370-377 ◽  
Author(s):  
I. Stuart Wood ◽  
Fátima Pérez de Heredia ◽  
Bohan Wang ◽  
Paul Trayhurn
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Responses ◽  
Strong Support ◽  
Low Grade ◽  
Tissue Mass ◽  
Diverse Range ◽  
Monocyte Chemoattractant Protein 1 ◽  
The Metabolic Syndrome ◽  
Adipose Tissue Dysfunction ◽  
Cellular Hypoxia

Expansion of adipose tissue mass, the distinctive feature of obesity, is associated with low-grade inflammation. White adipose tissue secretes a diverse range of adipokines, a number of which are inflammatory mediators (such as TNFα, IL-1β, IL-6, monocyte chemoattractant protein 1). The production of inflammatory adipokines is increased with obesity and these adipokines have been implicated in the development of insulin resistance and the metabolic syndrome. However, the basis for the link between increased adiposity and inflammation is unclear. It has been proposed previously that hypoxia may occur in areas within adipose tissue in obesity as a result of adipocyte hypertrophy compromising effective O2 supply from the vasculature, thereby instigating an inflammatory response through recruitment of the transcription factor, hypoxic inducible factor-1. Studies in animal models (mutant mice, diet-induced obesity) and cell-culture systems (mouse and human adipocytes) have provided strong support for a role for hypoxia in modulating the production of several inflammation-related adipokines, including increased IL-6, leptin and macrophage migratory inhibition factor production together with reduced adiponectin synthesis. Increased glucose transport into adipocytes is also observed with low O2 tension, largely as a result of the up-regulation of GLUT-1 expression, indicating changes in cellular glucose metabolism. Hypoxia also induces inflammatory responses in macrophages and inhibits the differentiation of preadipocytes (while inducing the expression of leptin). Collectively, there is strong evidence to suggest that cellular hypoxia may be a key factor in adipocyte physiology and the underlying cause of adipose tissue dysfunction contributing to the adverse metabolic milieu associated with obesity.

scholarly journals Follistatin-Like 1: A Potential Mediator of Inflammation in Obesity

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Nengguang Fan ◽  
Haiyan Sun ◽  
Yufan Wang ◽  
Yifei Wang ◽  
Lijuan Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Low Grade ◽  
Dependent Manner ◽  
Proinflammatory Mediators ◽  
Raw264.7 Macrophages ◽  
Potential Mediator ◽  
Obese Subjects

Obesity is associated with a state of chronic low-grade inflammation, which contributes to insulin resistance and type 2 diabetes. However, the molecular mechanisms that link obesity to inflammation are not fully understood. Follistatin-like 1 (FSTL1) is a novel proinflammatory cytokine that is expressed in adipose tissue and secreted by preadipocytes/adipocytes. We aimed to test whether FSTL1 could have a role in obesity-induced inflammation and insulin resistance. It was found that FSTL1 expression was markedly decreased during differentiation of 3T3-L1 preadipocytes but reinduced by TNF-α. Furthermore, a significant increase in FSTL1 levels was observed in adipose tissue of obese ob/ob mice, as well as in serum of overweight/obese subjects. Mechanistic studies revealed that FSTL1 induced inflammatory responses in both 3T3-L1 adipocytes and RAW264.7 macrophages. The expression of proinflammatory mediators including IL-6, TNF-α, and MCP-1 was upregulated by recombinant FSTL1 in a dose-dependent manner, paralleled with activation of the IKKβ-NFκB and JNK signaling pathways in the two cell lines. Moreover, FSTL1 impaired insulin signaling in 3T3-L1 adipocytes, as revealed by attenuated phosphorylation of both Akt and IRS-1 in response to insulin stimulation. Together, our results suggest that FSTL1 is a potential mediator of inflammation and insulin resistance in obesity.

scholarly journals Gestational Diabetes Mellitus and Infant Adiposity at Birth: A Systematic Review and Meta-Analysis of Therapeutic Interventions

2021 ◽  
Vol 10 (4) ◽  
pp. 835
Author(s):  
Manoja P. Herath ◽  
Jeffrey M. Beckett ◽  
Andrew P. Hills ◽  
Nuala M. Byrne ◽  
Kiran D. K. Ahuja
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fat Mass ◽  
Metabolic Disorders ◽  
Later Life ◽  
Therapeutic Interventions ◽  
Increased Risk ◽  
The Impact

Exposure to untreated gestational diabetes mellitus (GDM) in utero increases the risk of obesity and type 2 diabetes in adulthood, and increased adiposity in GDM-exposed infants is suggested as a plausible mediator of this increased risk of later-life metabolic disorders. Evidence is equivocal regarding the impact of good glycaemic control in GDM mothers on infant adiposity at birth. We systematically reviewed studies reporting fat mass (FM), percent fat mass (%FM) and skinfold thicknesses (SFT) at birth in infants of mothers with GDM controlled with therapeutic interventions (IGDMtr). While treating GDM lowered FM in newborns compared to no treatment, there was no difference in FM and SFT according to the type of treatment (insulin, metformin, glyburide). IGDMtr had higher overall adiposity (mean difference, 95% confidence interval) measured with FM (68.46 g, 29.91 to 107.01) and %FM (1.98%, 0.54 to 3.42) but similar subcutaneous adiposity measured with SFT, compared to infants exposed to normal glucose tolerance (INGT). This suggests that IGDMtr may be characterised by excess fat accrual in internal adipose tissue. Given that intra-abdominal adiposity is a major risk factor for metabolic disorders, future studies should distinguish adipose tissue distribution of IGDMtr and INGT.

scholarly journals Chemotactic cytokines, obesity and type 2 diabetes:in vivoandin vitroevidence for a possible causal correlation?

2009 ◽  
Vol 68 (4) ◽  
pp. 378-384 ◽  
Author(s):  
Henrike Sell ◽  
Jürgen Eckel
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Obese Patients ◽  
Tissue Mass ◽  
Tissue Biology ◽  
Wide Range ◽  
Adipose Tissue Mass

A strong causal link between increased adipose tissue mass and insulin resistance in tissues such as liver and skeletal muscle exists in obesity-related disorders such as type 2 diabetes. Increased adipose tissue mass in obese patients and patients with diabetes is associated with altered secretion of adipokines, which also includes chemotactic proteins. Adipose tissue releases a wide range of chemotactic proteins including many chemokines and chemerin, which are interesting targets for adipose tissue biology and for biomedical research in obesity and obesity-related diseases. This class of adipokines may be directly linked to a chronic state of low-grade inflammation and macrophage infiltration in adipose tissue, a concept intensively studied in adipose tissue biology in recent years. The inflammatory state of adipose tissue in obese patients may be the most important factor linking increased adipose tissue mass to insulin resistance. Furthermore, chemoattractant adipokines may play an important role in this situation, as many of these proteins possess biological activity beyond the recruitment of immune cells including effects on adipogenesis and glucose homeostasis in insulin-sensitive tissues. The present review provides a summary of experimental evidence of the role of adipose tissue-derived chemotactic cytokines and their function in insulin resistancein vivoandin vitro.

scholarly journals Adipose tissue inflammation and metabolic dysfunction: a clinical perspective

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Low Grade Inflammation

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).

scholarly journals Adipokines: inflammation and the pleiotropic role of white adipose tissue

2004 ◽  
Vol 92 (3) ◽  
pp. 347-355 ◽  
Author(s):  
Paul Trayhurn ◽  
I. Stuart Wood
Keyword(s):  
Adipose Tissue ◽  
Growth Factor ◽  
Inflammatory Cytokines ◽  
Acute Phase ◽  
White Adipose Tissue ◽  
Acute Phase Proteins ◽  
Endocrine Function ◽  
Low Grade ◽  
Circulating Levels

White adipose tissue is now recognised to be a multifunctional organ; in addition to the central role of lipid storage, it has a major endocrine function secreting several hormones, notably leptin and adiponectin, and a diverse range of other protein factors. These various protein signals have been given the collective name ‘adipocytokines’ or ‘adipokines’. However, since most are neither ‘cytokines’ nor ‘cytokine-like’, it is recommended that the term ‘adipokine’ be universally adopted to describe a protein that is secreted from (and synthesised by) adipocytes. It is suggested that the term is restricted to proteins secreted from adipocytes, excluding signals released only by the other cell types (such as macrophages) in adipose tissue. Theadipokinome(which together with lipid moieties released, such as fatty acids and prostaglandins, constitute thesecretomeof fat cells) includes proteins involved in lipid metabolism, insulin sensitivity, the alternative complement system, vascular haemostasis, blood pressure regulation and angiogenesis, as well as the regulation of energy balance. In addition, there is a growing list of adipokines involved in inflammation (TNFα, IL-1β, IL-6, IL-8, IL-10, transforming growth factor-β, nerve growth factor) and the acute-phase response (plasminogen activator inhibitor-1, haptoglobin, serum amyloid A). Production of these proteins by adipose tissue is increased in obesity, and raised circulating levels of several acute-phase proteins and inflammatory cytokines has led to the view that the obese are characterised by a state of chronic low-grade inflammation, and that this links causally to insulin resistance and the metabolic syndrome. It is, however, unclear as to the extent to which adipose tissue contributes quantitatively to the elevated circulating levels of these factors in obesity and whether there is a generalised or local state of inflammation. The parsimonious view is that the increased production of inflammatory cytokines and acute-phase proteins by adipose tissue in obesity relates primarily to localised events within the expanding fat depots. It is suggested that these events reflect hypoxia in parts of the growing adipose tissue mass in advance of angiogenesis, and involve the key controller of the cellular response to hypoxia, the transcription factor hypoxia inducible factor-1.

scholarly journals Deletion of Src family kinase Lyn aggravates endotoxin-induced lung inflammation

2015 ◽  
Vol 309 (11) ◽  
pp. L1376-L1381 ◽  
Author(s):  
Rong Gao ◽  
Zhongsen Ma ◽  
Mengshi Ma ◽  
Jinyan Yu ◽  
Jiao Chen ◽  
...  
Keyword(s):  
Tyrosine Kinases ◽  
Lung Inflammation ◽  
Inflammatory Responses ◽  
Pulmonary Inflammation ◽  
Inflammasome Activation ◽  
Inflammatory Signaling ◽  
Endotoxin Challenge ◽  
Proinflammatory Mediators ◽  
Src Family Tyrosine Kinases ◽  
Inhibitory Signaling

Overwhelming acute inflammation often leads to tissue damage during endotoxemia. In the present study, we investigated the role of Lyn, a member of the Src family tyrosine kinases, in modulating inflammatory responses in a murine model of endotoxemia. We examined lung inflammatory signaling in Lyn knockout (Lyn−/−) mice and wild-type littermates (Lyn+/+) during endotoxemia. Our data indicate that Lyn deletion aggravates endotoxin-induced pulmonary inflammation and proinflammatory signaling. We found increased activation of proinflammatory transcription factor NF-κB in the lung tissues of Lyn−/− mice after endotoxin challenge. Furthermore, during endotoxemia, the lung tissues of Lyn−/− mice showed increased inflammasome activation indicated by augmented caspase-1 and IL-1β cleavage and activation. The aggravated lung inflammatory signaling in Lyn−/− mice was associated with increased production of proinflammatory mediators and elevated matrix metallopeptidase 9 and reduced VE-cadherin levels. Our results suggest that Lyn kinase modulates inhibitory signaling to suppress endotoxin-induced lung inflammation.

scholarly journals Osteopontin – a multifunctional protein and its impact on an insulin resistance development

2014 ◽  
Vol 83 (2) ◽  
pp. 173-176
Author(s):  
Katarzyna Musialik ◽  
Damian Skrypnik ◽  
Paweł Bogdański ◽  
Monika Szulińska
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Inflammatory Process ◽  
Blood Stream ◽  
Interleukin 12 ◽  
Low Grade ◽  
Tissue Mass ◽  
Multifunctional Protein ◽  
Artery Disease ◽  
The Many

Osteopontin (OPN) is one of the many physiological elements creating human musculoskeletal system. It is suspected that this protein is one of the most important mediators responsible for osseous tissue mass resorption, regulated by parthormon. The origin of its name comes from one of its physiological action – rebuilding of the bone mass structure (osteo – bone, pontin – bridge). Osteopontin fulfils many different actions being secreted by many different types of cells, including macrophages, lymphocytes, epithelial cells, vascular smooth muscle cells, and osteoblasts. OPN plays an important part in inflammatory process. It provokes macrophages and dendritic cells to movement into the destination where inflammatory process takes place. It also stimulates macrophages to interleukin 12 (IL12) and interferon ? (IFN ?) secretion. Increased OPN concentration in blood stream might be regarded as a novel, independent indicator of coronary artery disease. Osteopontin plays an important role in macrophage infiltration of the adipose tissue and at the same time contributes to insulin resistance. Obesity induces chronic, low-grade tissue inflammation. Positive correlation was observed between body mass index (BMI) and number of macrophages accumulated in the fat tissue. Once aroused monocytes infiltrate the adipose tissue, which leads to persisting chronic inflammation. At the same time the excreted by them cytokines may be connected with the mechanisms of obesity-induced insulin resistance.

scholarly journals Cytosolic Self-DNA—A Potential Source of Chronic Inflammation in Aging

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3544
Author(s):  
Mansour Akbari ◽  
Daryl P. Shanley ◽  
Vilhelm A. Bohr ◽  
Lene Juel Rasmussen
Keyword(s):  
Innate Immunity ◽  
Chronic Inflammation ◽  
Inflammatory Responses ◽  
Experimental Models ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Innate Immune Responses ◽  
And Function ◽  
The Life Course ◽  
Cellular Components

Aging is the consequence of a lifelong accumulation of stochastic damage to tissues and cellular components. Advancing age closely associates with elevated markers of innate immunity and low-grade chronic inflammation, probably reflecting steady increasing incidents of cellular and tissue damage over the life course. The DNA sensing cGAS-STING signaling pathway is activated by misplaced cytosolic self-DNA, which then initiates the innate immune responses. Here, we hypothesize that the stochastic release of various forms of DNA from the nucleus and mitochondria, e.g., because of DNA damage, altered nucleus integrity, and mitochondrial damage, can result in chronic activation of inflammatory responses that characterize the aging process. This cytosolic self-DNA-innate immunity axis may perturb tissue homeostasis and function that characterizes human aging and age-associated pathology. Proper techniques and experimental models are available to investigate this axis to develop therapeutic interventions.

scholarly journals Epigenetic Regulation of Adipogenesis in Development of Metabolic Syndrome

2021 ◽  
Vol 8 ◽  
Author(s):  
Richa Pant ◽  
Priyanka Firmal ◽  
Vibhuti Kumar Shah ◽  
Aftab Alam ◽  
Samit Chattopadhyay
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Cancer Progression ◽  
Underlying Disease ◽  
Metabolic Health ◽  
Therapeutic Interventions ◽  
Tissue Mass ◽  
Epigenetic Events ◽  
Adipocyte Hypertrophy ◽  
Altered Gene

Obesity is one of the biggest public health concerns identified by an increase in adipose tissue mass as a result of adipocyte hypertrophy and hyperplasia. Pertaining to the importance of adipose tissue in various biological processes, any alteration in its function results in impaired metabolic health. In this review, we discuss how adipose tissue maintains the metabolic health through secretion of various adipokines and inflammatory mediators and how its dysfunction leads to the development of severe metabolic disorders and influences cancer progression. Impairment in the adipocyte function occurs due to individuals’ genetics and/or environmental factor(s) that largely affect the epigenetic profile leading to altered gene expression and onset of obesity in adults. Moreover, several crucial aspects of adipose biology, including the regulation of different transcription factors, are controlled by epigenetic events. Therefore, understanding the intricacies of adipogenesis is crucial for recognizing its relevance in underlying disease conditions and identifying the therapeutic interventions for obesity and metabolic syndrome.

Sign in / Sign up

Export Citation Format

Share Document