scholarly journals microRNAs as a New Mechanism Regulating Adipose Tissue Inflammation in Obesity and as a Novel Therapeutic Strategy in the Metabolic Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Qian Ge ◽  
Sonia Brichard ◽  
Xu Yi ◽  
QiFu Li
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Therapeutic Strategy ◽  
Molecular Mechanisms ◽  
Inflammatory Mediator ◽  
Primary Site ◽  
The Metabolic Syndrome ◽  
Metabolic Endotoxemia ◽  
Mediate Inflammation

Obesity is associated closely with the metabolic syndrome (MS). It is well known that obesity-induced chronic inflammation plays a fundamental role in the pathogenesis of MS. White adipose tissue (AT) is the primary site for the initiation and exacerbation of obesity-associated inflammation. Exploring the mechanisms of white AT inflammation and resetting the immunological balance in white AT could be crucial for the management of MS. Several prominent molecular mechanisms have been proposed to mediate inflammation in white AT, including hypoxia, endoplasmic reticulum stress, lipotoxicity, and metabolic endotoxemia. Recently, a growing body of evidence supports the role of miRNAs as a new important inflammatory mediator by regulating both the adaptive and innate immunity. This review will focus on the implication of miRNAs in white AT inflammation in obesity, and will also highlight the potential of miRNAs as targets for therapeutic intervention in MS as well as the challenges lying in miRNA-targeting therapeutics.

The Role of Adipose Tissue Hypercortisolemia in the Development of the Metabolic Syndrome in Severely Obese Patients.

2010 ◽  
pp. P2-467-P2-467
Author(s):  
M Michalaki ◽  
V Kyriazopoulou ◽  
A Antonacopoulou ◽  
M Nikolaou ◽  
A Tsoukas ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Obese Patients ◽  
The Metabolic Syndrome ◽  
Severely Obese

scholarly journals The Role of Plasminogen Activator Inhibitor-1 in the Metabolic Syndrome and Its Regulation

2014 ◽  
Vol 3 (6) ◽  
pp. 36 ◽  
Author(s):  
Martha Phelan ◽  
David M. Kerins
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
The Metabolic Syndrome ◽  
Activator Inhibitor ◽  
Pai 1

<p>Obesity is a major risk factor for cardiovascular disease (CVD). Lipid abnormalities, hypertension, impaired glucose tolerance or diabetes, are cardiovascular risk factors that are frequently present in patients with obesity. Haemostatic and fibrinolytic disturbances are also considered to be important risk factors for CVD hence, a potential link between CVD, obesity and the metabolic syndrome arises. Regulation of the fibrinolytic system can occur at the level of plasminogen activators and plasminogen activator inhibitor-1 (PAI-1). PAI-1, a glycoprotein, is one of the most important inhibitors of fibrinolysis. Regulation of this serine protease inhibitor may have a beneficial effect on other conditions associated with the metabolic syndrome. Human adipose tissue is a source of PAI-1. PAI-1 production may in turn be controlled by a number of hormones and cytokines which are secreted by adipose tissue in addition to dietary factors. In this review we summarise the current knowledge regarding the role of altered fibrinolytic function in obesity, CVD and hence the metabolic syndrome. Regulatory factors including different dietary components, weight loss and dietary intervention will also be discussed.</p>

scholarly journals Stress in Obesity and Associated Metabolic and Cardiovascular Disorders

Scientifica ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Paul Holvoet
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Molecular Mechanisms ◽  
Chronic Inflammatory Disease ◽  
Stress Conditions ◽  
Cardiovascular Disorders ◽  
Control Mechanisms ◽  
Complex Disorder ◽  
The Metabolic Syndrome

Obesity has significant implications for healthcare, since it is a major risk factor for both type 2 diabetes and the metabolic syndrome. This syndrome is a common and complex disorder combining obesity, dyslipidemia, hypertension, and insulin resistance. It is associated with high atherosclerotic cardiovascular risk, which can only partially be explained by its components. Therefore, to explain how obesity contributes to the development of metabolic and cardiovascular disorders, more and better insight is required into the effects of personal and environmental stress on disease processes. In this paper, we show that obesity is a chronic inflammatory disease, which has many molecular mechanisms in common with atherosclerosis. Furthermore, we focus on the role of oxidative stress associated with obesity in the development of the metabolic syndrome. We discuss how several stress conditions are related to inflammation and oxidative stress in association with obesity and its complications. We also emphasize the relation between stress conditions and the deregulation of epigenetic control mechanisms by means of microRNAs and show how this impairment further contributes to the development of obesity, closing the vicious circle. Finally, we discuss the limitations of current anti-inflammation and antioxidant therapy to treat obesity.

Metabolic Syndrome, a Cardiovascular Disease Risk Factor: Role of Adipocytokines and Impact of Diet and Physical Activity

2004 ◽  
Vol 29 (6) ◽  
pp. 808-829 ◽  
Author(s):  
Lindsay E. Robinson ◽  
Terry E. Graham
Keyword(s):  
Physical Activity ◽  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Key Words Insulin ◽  
Diet And Physical Activity ◽  
The Impact

The metabolic syndrome comprises an array of cardiovascular disease (CVD) risk factors such as abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Insulin resistance and/or increased abdominal (visceral) obesity have been suggested as potential etiological factors. More recently, increasing evidence has associated insulin resistance and subclinical inflammation involving cytokines derived from adipose tissue, or adipocytokines. Despite the fact that precise mechanisms have yet to be established, there is a significant role for both diet and physical activity to improve the many factors associated with the metabolic syndrome, including modulation of various adipocytokines. Although both diet and physical activity have been studied for their ability to modify cytokines in more traditional inflammatory conditions, such as rheumatoid arthritis, they have been less studied in relation to inflammation as an underlying cause of the metabolic syndrome and/or CVD. A more thorough understanding of the clustering of metabolic abnormalities and their underlying etiology will help to define diet and physical activity guidelines for preventing and treating the metabolic syndrome, an important aspect of CVD prevention. This paper will address potential underlying causes of the metabolic syndrome, with a focus on the putative mechanistic role of adipocytokines, and will discuss the impact of diet and physical activity on the metabolic syndrome. Key words: insulin resistance syndrome, obesity, adipose tissue, skeletal muscle, cytokines, TNF-α, IL-6, PAI-1, inflammation, nutrition, exercise

Metabolic syndrome, inflammation and atherothrombosis

2013 ◽  
Vol 33 (04) ◽  
pp. 283-294 ◽  
Author(s):  
T. W. Weiss ◽  
M. Rohla
Keyword(s):  
Physical Activity ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Atherosclerotic Plaques ◽  
Traditional Concept ◽  
The Past ◽  
The Metabolic Syndrome ◽  
Inflammatory Pattern

SummaryExtensive research of the past decades altered our traditional concept about the genesis of atherosclerosis fundamentally. Today, the crucial role of inflammation in the formation and progression of atherosclerotic plaques is indisputable. Patients at high risk for developing cardiovascular disease, owing to poor diet, obesity and low physical activity have been shown to exhibit a particular inflammatory pattern.Therefore, the present review highlights the crosslink between the metabolic syndrome (MetS), adipose tissue, adipokines and selected inflammatory cytokines in the context of atherothrombosis and cardiovascular disease.

Mammary adipose tissue and cancer cell growth: The role of adipose tissue in the tumor microenvironment

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22009-e22009
Author(s):  
P. A. Carroll ◽  
L. Healy ◽  
J. Lysaght ◽  
M. Griffin ◽  
B. Dunne ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metabolic Syndrome ◽  
Cell Proliferation ◽  
Adipose Tissue ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
The Metabolic Syndrome ◽  
Proliferation Response

e22009 Background: Worldwide, the prevalence of obesity is rapidly increasing, correlating with a direct increase in cancer rates1. Adipose tissue is considered an important endocrine organ producing several important hormones and cytokines including leptin and adiponectin. Mechanisms for the role of obesity in cancer states includes the excess or unregulated secretion of adipocytokines from adipose tissue, and potentially the metabolic syndrome (a cluster of co-morbidities linked to metabolic dysregulation). Mammary adipose tissue is proposed to play a vital role in the microenvironment of normal and tumour states within the breast2. Breast adipose tissue is a good candidate to investigate effects of obesity and metabolic disturbances on cancer states. Methods: Peritumoural (PT) adipose tissue adjacent to the tumour and distal adipose tissue (D) within the breast was sampled in 10 patients. The tissue was processed and cultured for 72hrs in serum free minimal cytokine media. A-MB-231 and MCF-7 breast cancer cell lines were then cultured with this adipocyte conditioned media (ACM) and cell proliferation response was then measured using BrDU assays. The adipocytokine profile at the mRNA and protein level was measured in ACM and adipose tissue for comparative differences using RT-PCR, ELISA and Cytokine Profiler technology. Results: ACM from both sites promoted tumour cell survival. There was however, a differential cell proliferation response noted between the peritumoural (PT) ACM and that from the distant (D) ACM. Pro-inflammatory mediators (VEGF, TNF-α, EGF) were also demonstrated a trend to be differentially expressed between the 2 sites. Conclusions: Proliferation of breast cancer cell lines occurs in response to ACM, with differential effects seen between peritumoural ACM and distant ACM. This may be mediated through increased pro-inflammatory or pro- mitogenic adipocytokine production in adipose tissue surrounding tumour. Further analysis will determine what role obesity and the metabolic syndrome plays in the results noted. No significant financial relationships to disclose.

scholarly journals Metabolic syndrome and Cancer: Do they share common molecular pathways?

2016 ◽  
Vol 7 (2) ◽  
pp. 7-15
Author(s):  
E. Veniou ◽  
I. Sofatzis ◽  
I. Kalantzis ◽  
M. Karakosta ◽  
M. Logothetis ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Molecular Mechanisms ◽  
Clinical Evidence ◽  
Lifestyle Changes ◽  
Dietary Quality ◽  
The Metabolic Syndrome ◽  
Risk Of Cancer ◽  
Clustering Of Risk Factors

Abstract Metabolic syndrome, a clustering of risk factors including obesity, has emerged as a global health plague. A lot of epidemiological and clinical evidence suggests that the metabolic syndrome is linked not only to cardiovascular diseases and diabetes mellitus type 2 but also to cancer development and progression. In this review the potential mechanisms tying the metabolic syndrome with cancer are presented. The role of insulin resistance and hyperinsulinemia, the activation of insulin-like growth factor-1 (IGF-1) pathway, and the induction of cytotoxic products are highlighted. Subsequent effects leading to oxidative stress, release of lipokines with signaling properties by adipocytes, development of a sustained systemic inflammation, production of inflammatory cytokines, and establishment of a tumorigenic environment are also discussed. The importance of the metabolic syndrome and obesity coupled with the deeper understanding of the underlying molecular mechanisms has trigger intensive clinical research with an aim to prevent the risk of cancer and improve outcomes. Moreover, the need for lifestyle changes with increased physical activity and improved dietary quality has been emerged as urgent health priority.

scholarly journals DISORDER OF INTERCELLULAR CORRELATIONS IN PATHOGENESIS OF FATTY TISSUE INFLAMMATION IN METABOLIC SYNDROME

2013 ◽  
Vol 12 (6) ◽  
pp. 144-153 ◽  
Author(s):  
I. A. Osikhov ◽  
I. D. Bespalova ◽  
V. A. Bychkov ◽  
N. V. Ryazantseva ◽  
V. V. Kalyuzhin ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Molecular Mechanisms ◽  
Fatty Tissue ◽  
Scientific Review ◽  
Tissue Inflammation ◽  
The Metabolic Syndrome ◽  
Pathological Conditions ◽  
Symptom Complex ◽  
Main Component

Due to the fact that nowadays mechanisms of syntropy of pathological conditions and nosological units, united within the metabolic syndrome, remain unclear, the scientific review attempts to summarize data on the role of fatty tissue inflammation in pathogenesis of this symptom complex. The results of recent major foreign studies on evaluation of pro-inflammatory activity of adipocytes and macrophages of the fatty tissue, as well as the data on peculiarities of their interactions in abdominal obesity, which is the main component of the metabolic syndrome, were analyzed. Studing pathogenesis of fatty tissue inflammation from the perspective of evaluation of disorders in cell cooperation will allow to more deeply understand cellular and molecular mechanisms of this process as well as open new avenues for developing new pathogenetically justified approaches to metabolic syndrome treatment.

scholarly journals MicroRNAs: The Link Between the Metabolic Syndrome and Oncogenesis

2021 ◽  
Vol 22 (12) ◽  
pp. 6337
Author(s):  
Adriana Fodor ◽  
Andrada Luciana Lazar ◽  
Cristina Buchman ◽  
Brandusa Tiperciuc ◽  
Olga Hilda Orasan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Cancer Progression ◽  
The Metabolic Syndrome ◽  
Cancer Pathogenesis ◽  
Non Coding Rna ◽  
Target Therapies ◽  
Inflammatory State ◽  
Type Two Diabetes

Metabolic syndrome (MetS) represents a cluster of disorders that increase the risk of a plethora of conditions, in particular type two diabetes, cardiovascular diseases, and certain types of cancers. MetS is a complex entity characterized by a chronic inflammatory state that implies dysregulations of adipokins and proinflammatory cytokins together with hormonal and growth factors imbalances. Of great interest is the implication of microRNA (miRNA, miR), non-coding RNA, in cancer genesis, progression, and metastasis. The adipose tissue serves as an important source of miRs, which represent a novel class of adipokines, that play a crucial role in carcinogenesis. Altered miRs secretion in the adipose tissue, in the context of MetS, might explain their implication in the oncogenesis. The interplay between miRs expressed in adipose tissue, their dysregulation and cancer pathogenesis are still intriguing, taking into consideration the fact that miRNAs show both carcinogenic and tumor suppressor effects. The aim of our review was to discuss the latest publications concerning the implication of miRs dysregulation in MetS and their significance in tumoral signaling pathways. Furthermore, we emphasized the role of miRNAs as potential target therapies and their implication in cancer progression and metastasis.

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