scholarly journals THU0520 DIFFUSE ENTHESITIS AND LOW-GRADE INFLAMMATION IN PATIENTS WITH METABOLIC SYNDROME: A CLINICAL AND ULTRASOUND STUDY.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 499.1-499
Author(s):  
P. Falsetti ◽  
E. Conticini ◽  
C. Baldi ◽  
M. Bardelli ◽  
S. Gentileschi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Structural Damage ◽  
Power Doppler ◽  
Older Age ◽  
Low Grade ◽  
High Prevalence ◽  
The Us ◽  
Inflammatory State

Background:Metabolic syndrome (MS) is a clinical condition characterized by central obesity and additional factors such dyslipidemia, hypertension, raised fasting plasma. Scanty observations describe the association of MS with musculoskeletal conditions, such as enthesopathies and diffuse idiopathic hyperostosis syndrome (DISH). Musculoskeletal ultrasound (US) has been applied to the study of entheses, but the real prevalence and characteristics of entheseal involvement in MS has yet to be clarified.Objectives:The aim of our work was to study the US-defined entheseal changes in MS, to correlates the US enthesitis scores to clinical characteristics, and to define a relation between MS-related enthesitis and the presence of concurrent DISHMethods:Sixty consecutive outpatients (24 males, 36 females, mean age 60 years), all fullfilling International Diabetes Foundation (IDF) criteria for MS, were also evaluated with multi-site bilateral US entheseal examination. Each patient underwent power Doppler (PD) US examination of twelve entheseal sites, using Esaote MyLab Twice with 6–18 MHz transducer. Enthesitis was defined on the basis of OMERACT’s filter. Inflammatory and structural changes were scored as a whole when present (score 1) or absent (score 0). The sum of entheses with inflammatory and structural damage was defined as “global inflammatory score” (GIs) and “global structural damage score” (GSDs) for each patient. The Leeds Enthesitis Index (LEI) was also applied, and a spinal radiography was obtained for each patient to research concurrent signs of DISH satisfying Resnick and Niwayama criteria.Results:Patients showed moderate overweight (mean BMI 29) and a diagnosis of type 2 diabetes was present in 24 (40%). A low-grade inflammatory state was demonstrated in MS (mean CRP 0,58 md/dL, mean ESR 21,9 mm/h). A high prevalence of US-defined enthesitis was noted in 52 patients (86%) and 127/720 entheses (17,6%). PD signals, were reported in 11 patients (18%) and 11/720 entheses (1,52%), and they were associated to clinical symptoms expressed as LEI (p=0,0138). Erosions, although rare (0.3% of entheses), were more frequent in males (p= 0.001). Moreover, in 57 patients (95%) and 217 entheses (30%) structural damages were found. A correlation was found between GIs and GSDs and both BMI (p=0.0233 and p=0.0068 respectively), LEI (p=0.03 and p=0.0099 respectively), and type 2 diabetes (p=0.0248 and p=0.0156 respectively). In 28 patients (46%) a concurrent diagnosis of DISH was made. In multivariate regression analysis the best predictors for DISH were higher levels of CRP (p=0,038) and older age (p<0,0001). DISH correlated with older age (p<0,0001), CRP and ESR (p= 0,0428 p=0,0069 respectively) and US global scores for enthesitis (p=0,0312 for GIs, p=0,0071 for GSDs).Conclusion:This is the first study where diffuse enthesitis and entheseal structural damage are demonstrated with high prevalences in MS, comparable or also higher than those reported for SpA-related enthesitis. Our data, obtained using the most recent OMERACT’s definition for US-detected enthesitis (proposed for SpA), also suggest a low specificity of this definition, in consideration of the high prevalence of MS-associated enthesitis. Moreover PD was associated to entheseal pain expressed as LEI. Both GIs and GSDs showed a correlation with overweight and type 2 diabetes. As secondary result, this study demonstrated that almost half of patients with MS could have a concurrent diagnosis of DISH. Patients with DISH were older, with higher levels of inflammation, and higher scores of US-defined enthesitis. Our results suggest that MS and DISH could be strictly related; diffuse enthesitis with a low-grade inflammatory state should be regarded as potential factor of progression from MS towards a conclamed DISH.Disclosure of Interests:None declared

scholarly journals Peroxisome Proliferator-Activated Receptor γ and Adipose Tissue—Understanding Obesity-Related Changes in Regulation of Lipid and Glucose Metabolism

2006 ◽  
Vol 92 (2) ◽  
pp. 386-395 ◽  
Author(s):  
Arya M. Sharma ◽  
Bart Staels
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Endocrine Function ◽  
Low Grade ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Abstract Context: Adipose tissue is a metabolically dynamic organ, serving as a buffer to control fatty acid flux and a regulator of endocrine function. In obese subjects, and those with type 2 diabetes or the metabolic syndrome, adipose tissue function is altered (i.e. adipocytes display morphological differences alongside aberrant endocrine and metabolic function and low-grade inflammation). Evidence Acquisition: Articles on the role of peroxisome proliferator-activated receptor γ (PPARγ) in adipose tissue of healthy individuals and those with obesity, metabolic syndrome, or type 2 diabetes were sourced using MEDLINE (1990–2006). Evidence Synthesis: Articles were assessed to provide a comprehensive overview of how PPARγ-activating ligands improve adipose tissue function, and how this links to improvements in insulin resistance and the progression to type 2 diabetes and atherosclerosis. Conclusions: PPARγ is highly expressed in adipose tissue, where its activation with thiazolidinediones alters fat topography and adipocyte phenotype and up-regulates genes involved in fatty acid metabolism and triglyceride storage. Furthermore, PPARγ activation is associated with potentially beneficial effects on the expression and secretion of a range of factors, including adiponectin, resistin, IL-6, TNFα, plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, and angiotensinogen, as well as a reduction in plasma nonesterified fatty acid supply. The effects of PPARγ also extend to macrophages, where they suppress production of inflammatory mediators. As such, PPARγ activation appears to have a beneficial effect on the relationship between the macrophage and adipocyte that is distorted in obesity. Thus, PPARγ-activating ligands improve adipose tissue function and may have a role in preventing progression of insulin resistance to diabetes and endothelial dysfunction to atherosclerosis.

The Role of Diet in Patients with Metabolic Syndrome

2019 ◽  
Vol 26 (19) ◽  
pp. 3613-3619 ◽  
Author(s):  
Paloma Almeda-Valdes ◽  
Roberto J. Herrera-Mercadillo ◽  
Carlos A. Aguilar-Salinas ◽  
Misael Uribe ◽  
Nahum Méndez-Sánchez
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Coronary Heart Disease ◽  
Dietary Fat ◽  
Lifestyle Modification ◽  
Fat Intake ◽  
High Prevalence

Metabolic syndrome is a frequent metabolic disorder characterized by obesity and insulin resistance seems to be the main pathophysiological alteration. The goal of treating metabolic syndrome is to reduce the risk of coronary heart disease and the development of type 2 diabetes. The lifestyle modification therapy combines specific recommendations on diet alone or combined with other strategies. In this review, we address the following topics: 1) the importance of the high prevalence of metabolic syndrome and obesity, and 2) the role of lifestyle modification focusing on dietary fat intake in the management of MS.

scholarly journals Cardiac Autonomic Neuropathy: A Progressive Consequence of Chronic Low-Grade Inflammation in Type 2 Diabetes and Related Metabolic Disorders

2020 ◽  
Vol 21 (23) ◽  
pp. 9005
Author(s):  
Nour-Mounira Z. Bakkar ◽  
Haneen S. Dwaib ◽  
Souha Fares ◽  
Ali H. Eid ◽  
Yusra Al-Dhaheri ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Autonomic Neuropathy ◽  
Experimental Models ◽  
Cardiac Autonomic Neuropathy ◽  
Low Grade ◽  
Metabolic Inflammation ◽  
The Metabolic Syndrome ◽  
Cardiovascular Morbidity And Mortality

Cardiac autonomic neuropathy (CAN) is one of the earliest complications of type 2 diabetes (T2D), presenting a silent cause of cardiovascular morbidity and mortality. Recent research relates the pathogenesis of cardiovascular disease in T2D to an ensuing chronic, low-grade proinflammatory and pro-oxidative environment, being the hallmark of the metabolic syndrome. Metabolic inflammation emerges as adipose tissue inflammatory changes extending systemically, on the advent of hyperglycemia, to reach central regions of the brain. In light of changes in glucose and insulin homeostasis, dysbiosis or alteration of the gut microbiome (GM) emerges, further contributing to inflammatory processes through increased gut and blood–brain barrier permeability. Interestingly, studies reveal that the determinants of oxidative stress and inflammation progression exist at the crossroad of CAN manifestations, dictating their evolution along the natural course of T2D development. Indeed, sympathetic and parasympathetic deterioration was shown to correlate with markers of adipose, vascular, and systemic inflammation. Additionally, evidence points out that dysbiosis could promote a sympatho-excitatory state through differentially affecting the secretion of hormones and neuromodulators, such as norepinephrine, serotonin, and γ-aminobutyric acid, and acting along the renin–angiotensin–aldosterone axis. Emerging neuronal inflammation and concomitant autophagic defects in brainstem nuclei were described as possible underlying mechanisms of CAN in experimental models of metabolic syndrome and T2D. Drugs with anti-inflammatory characteristics provide potential avenues for targeting pathways involved in CAN initiation and progression. The aim of this review is to delineate the etiology of CAN in the context of a metabolic disorder characterized by elevated oxidative and inflammatory load.

scholarly journals Dietary fatty acids on aortic root calcification in mice with metabolic syndrome

2017 ◽  
Vol 8 (4) ◽  
pp. 1468-1474 ◽  
Author(s):  
Maria C. Naranjo ◽  
Beatriz Bermudez ◽  
Indara Garcia ◽  
Sergio Lopez ◽  
Rocio Abia ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Aortic Root ◽  
Dietary Fatty Acids ◽  
Low Grade ◽  
Low Grade Inflammation

Metabolic syndrome (MetS) is associated with obesity, dyslipidemia, type 2 diabetes, and chronic low-grade inflammation.

Gut microbiota in health and disease: an overview focused on metabolic inflammation

2016 ◽  
Vol 7 (2) ◽  
pp. 181-194 ◽  
Author(s):  
R. Nagpal ◽  
M. Kumar ◽  
A.K. Yadav ◽  
R. Hemalatha ◽  
H. Yadav ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Adverse Outcomes ◽  
Special Focus ◽  
Low Grade ◽  
Immune Functions ◽  
Metabolic Inflammation

In concern to the continuously rising global prevalence of obesity, diabetes and associated diseases, novel preventive and therapeutic approaches are urgently required. However, to explore and develop such innovative strategies, a meticulous comprehension of the biological basis of these diseases is extremely important. Past decade has witnessed an enormous amount of research investigation and advancement in the field of obesity, diabetes and metabolic syndrome, with the gut microbiota receiving a special focus in the triangle of nutrition, health and diseases. In particular, the role of gut microbiota in health and diseases has been one of the most vigorous and intriguing field of recent research; however, much still remains to be elucidated about its precise role in host metabolism and immune functions and its implication in the onset, progression as well as in the amelioration of metabolic ailments. Recent investigations have suggested a significant contribution of the gut microbiota in the regulation and impairment of energy homeostasis, thereby causing metabolic disorders, such as metabolic endotoxemia, insulin resistance and type 2 diabetes. Numerous inflammatory biomarkers have been found to be associated with obesity, diabetes and risk of other associated adverse outcomes, thereby suggesting that a persistent low-grade inflammatory response is a potential risk factor. In this milieu, this review intends to discuss potential evidences supporting the disturbance of the gut microbiota balance and the intestinal barrier permeability as a potential triggering factor for systemic inflammation in the onset and progression of obesity, type 2 diabetes and metabolic syndrome.

scholarly journals Evaluate the effects of metabolic syndrome in adolescents and children

2020 ◽  
Vol 7 (3) ◽  
pp. 287-292
Author(s):  
Rui-Min Jia ◽  
Xiao-Ning Yan ◽  
Jing Sun
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Obese Children ◽  
The Metabolic Syndrome ◽  
Disease Outcomes ◽  
High Prevalence ◽  
Underlying Pathophysiology

AbstractThe metabolic syndrome (MS) in adolescents and children can cause serious consequences that lead researchers to pay efforts to study in such area. Presently, MS definition is still not standardized. Different versions of MS definition have been used by numerous studies, which may be a problem to identify MS and then to predict and prevent clinical diseases. The pediatric literature shows that insulin resistance and obesity might be the key underlying pathophysiology of MS to cause many related diseases. High prevalence of MS is in overweight and obese children and adolescents. This article focuses on such above issues and also effects of MS on two main disease outcomes: cardiovascular disease and type 2 diabetes.

scholarly journals The role of IL-1 in the regulation of copeptin in patients with metabolic syndrome

2020 ◽  
Vol 9 (7) ◽  
pp. 715-723
Author(s):  
Milica Popovic ◽  
Fahim Ebrahimi ◽  
Sandrine Andrea Urwyler ◽  
Marc Yves Donath ◽  
Mirjam Christ-Crain
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Surrogate Marker ◽  
Low Grade ◽  
Double Blind Study ◽  
Double Blind ◽  
Protein Levels ◽  
Reactive Protein ◽  
Low Grade Inflammation

Arginine vasopressin (AVP) was suggested to contribute to cardiovascular risk and type 2 diabetes in patients with metabolic syndrome. The proinflammatory cytokine interleukin (IL)-1 is able to induce AVP secretion and plays a causal role in cardiovascular mortality and type 2 diabetes. We investigated in two studies whether copeptin levels – the surrogate marker for AVP – are regulated by IL-1-mediated chronic inflammation in patients with metabolic syndrome. Study A was a prospective, interventional, single-arm study (2014–2016). Study B was a randomized, placebo-controlled, double-blind study (2016–2017). n = 73 (Study A) and n = 66 (Study B) adult patients with metabolic syndrome were treated with 100 mg anakinra or placebo (only in study B) twice daily for 1 day (study A) and 28 days (study B). Fasting blood samples were drawn at day 1, 7, and 28 of treatment for measurement of serum copeptin. Patients with chronic low-grade inflammation (C-reactive protein levels ≥2 mg/L) and BMI >35 kg/m2 had higher baseline copeptin levels (7.7 (IQR 4.9–11.9) vs 5.8 (IQR 3.9–9.3) pmol/L, Pinflamm = 0.009; 7.8 (IQR 5.4–11.7) vs 4.9 (IQR 3.7–9.8) pmol/L, PBMI = 0.008). Copeptin levels did not change either in the anakinra or in the placebo group and remained stable throughout the treatment (P = 0.44). Subgroup analyses did not reveal effect modifications. Therefore, we conclude that, although IL-1-mediated inflammation is associated with increased circulating copeptin levels, antagonizing IL-1 does not significantly alter copeptin levels in patients with metabolic syndrome.

AGEING WITHOUT DISEASES

2019 ◽  
pp. 123-131
Author(s):  
А.А. Пальцын
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Cardiovascular Diseases ◽  
Respiratory Diseases ◽  
Older Age ◽  
Modern World ◽  
Syndrome Type ◽  
Chronic Respiratory Diseases

Наиболее распространенные неинфекционные болезни современного мира: метаболический синдром, диабет 2-го типа, хронические респираторные заболевания, церебро- и кардиоваскулярные болезни, болезнь Альцгеймера и другие деменции, депрессии, опухоли, саркопения, остеопороз имеют общий механизм нарушения гомеостаза - окислительный стресс. Другая, объединяющая эти болезни черта - пожилой и старческий возраст пациентов. Связываются эти характеристики снижением адаптивных способностей организма, развивающемся по мере увеличения числа прожитых лет. Связь, в принципе, неизбежная, но в конкретности поддающаяся, как всё живое, влиянию среды. В статье представлены некоторые наиболее известные приемы создания такой среды (образа жизни), которые могут исключить или отодвинуть (нередко на годы) начало болезней. The most common noninfectious diseases of the modern world, including metabolic syndrome, type 2 diabetes, chronic respiratory diseases, cerebrovascular and cardiovascular diseases, Alzheimer’s disease and other dementias, depression, tumors, sarcopenia, and osteoporosis, share a mechanism of homeostatic disorders, oxidative stress. Another common feature of these diseases is the old and senile age of patients. These characteristics are linked with impaired adaptability, which develops with older age. In principle, this combination is inevitable but the environment can influence it like all life. The article presents some of the most well-known techniques for creating such an environment (lifestyle) that could exclude or postpone (often for years) the onset of disease.

scholarly journals Inflammation as a Link between Obesity and Metabolic Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Faloia Emanuela ◽  
Michetti Grazia ◽  
De Robertis Marco ◽  
Luconi Maria Paola ◽  
Furlani Giorgio ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Visceral Obesity ◽  
Low Grade ◽  
Subsequent Increase ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Inflammatory State

The metabolic syndrome is a complex of clinical features leading to an increased risk for cardiovascular disease and type 2 diabetes mellitus in both sexes. Visceral obesity and insulin resistance are considered the main features determining the negative cardiovascular profile in metabolic syndrome. The aim of this paper is to highlight the central role of obesity in the development of a chronic low-grade inflammatory state that leads to insulin resistance, endothelial and microvascular dysfunctions. It is thought that the starting signal of this inflammation is overfeeding and the pathway origins in all the metabolic cells; the subsequent increase in cytokine production recruits immune cells in the extracellular environment inducing an overall systemic inflammation. This paper focuses on the molecular and cellular inflammatory mechanisms studied until now.

scholarly journals Anti-Inflammatory Strategies Targeting Metaflammation in Type 2 Diabetes

Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2224 ◽  
Author(s):  
Alina Kuryłowicz ◽  
Krzysztof Koźniewski
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Low Grade ◽  
Peripheral Tissues ◽  
Inflammatory State ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Immunomodulatory Therapies

One of the concepts explaining the coincidence of obesity and type 2 diabetes (T2D) is the metaflammation theory. This chronic, low-grade inflammatory state originating from metabolic cells in response to excess nutrients, contributes to the development of T2D by increasing insulin resistance in peripheral tissues (mainly in the liver, muscles, and adipose tissue) and by targeting pancreatic islets and in this way impairing insulin secretion. Given the role of this not related to infection inflammation in the development of both: insulin resistance and insulitis, anti-inflammatory strategies could be helpful not only to control T2D symptoms but also to treat its causes. This review presents current concepts regarding the role of metaflammation in the development of T2D in obese individuals as well as data concerning possible application of different anti-inflammatory strategies (including lifestyle interventions, the extra-glycemic potential of classical antidiabetic compounds, nonsteroidal anti-inflammatory drugs, immunomodulatory therapies, and bariatric surgery) in the management of T2D.

Sign in / Sign up

Export Citation Format

Share Document