Implications of resistin plasma levels in subjects undergoing coronary angiography

Pilz, Stefan; Weihrauch, Gisela; Seelhorst, Ursula; Wellnitz, Britta; Winkelmann, Bernhard R.; Boehm, Bernhard O.; März, Winfried

doi:10.1111/j.1365-2265.2007.02743.x

Cited by 43 publications

(44 citation statements)

References 38 publications

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“…In contrast, no relationship between Resistin levels and CAD was found among 1161 subjects in the LU-RIC study [113] . Moreover, Resistin was not associated with cardiovascular mortality.…”

Section: Resistinmentioning

confidence: 76%

Adipose tissue and vascular inflammation in coronary artery disease

Golia¹,

Limongelli²,

Natale³

et al. 2014

WJC

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Obesity has become an important public health issue in Western and developing countries, with well known metabolic and cardiovascular complications. In the last decades, evidence have been growing about the active role of adipose tissue as an endocrine organ in determining these pathological consequences. As a consequence of the expansion of fat depots, in obese subjects, adipose tissue cells develope a phenotypic modification, which turns into a change of the secretory output. Adipocytokines produced by both adipocytes and adipose stromal cells are involved in the modulation of glucose and lipid handling, vascular biology and, moreover, participate to the systemic inflammatory response, which characterizes obesity and metabolic syndrome. This might represent an important pathophysiological link with atherosclerotic complications and cardiovascular events. A great number of adipocytokines have been described recently, linking inflammatory mileu and vascular pathology. The understanding of these pathways is crucial not only from a pathophysiological point of view, but also to a better cardiovascular disease risk stratification and to the identification of possible therapeutic targets. The aim of this paper is to review the role of Adipocytokines as a possible link between obesity and vascular disease. Key words: Adipocytokines; Obesity; Metabolic syndrome; Coronary artery disease; Inflammation Core tip: Our article, provide a comprehensive review of the evidence about adipose tissue and cardiovascular risk, focusing on the pathophysiological and clinical role of fat-derived mediators, the so-called adipocytokines.

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“…In contrast, no relationship between Resistin levels and CAD was found among 1161 subjects in the LU-RIC study [113] . Moreover, Resistin was not associated with cardiovascular mortality.…”

Section: Resistinmentioning

confidence: 76%

Adipose tissue and vascular inflammation in coronary artery disease

Golia¹,

Limongelli²,

Natale³

et al. 2014

WJC

View full text Add to dashboard Cite

show abstract

“…High resistin level appears to be associated with poor outcome after atherothrombotic ischemic stroke, independently of other adverse predictors (Efstathiou et al, 2007). However, some studies have not detected an association between elevated circulating resistin level and either prevalence or outcome of CAD (Yaturu et al, 2006;Hoefle et al, 2007;Pilz et al, 2007;Piestrzeniewicz et al, 2008). The discrepancy between study results could be related to differing demographics of the study groups, study design and patient selection criteria and also to non-standardized assay method.…”

Section: Human Resistin In Atherosclerosis and Coronary Artery Diseasementioning

confidence: 99%

Human resistin in cardiovascular disease

Lee

Kim

2012

J. Smooth Muscle Res.

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An adipokine, resistin, was first discovered as a potential mediator of obesity related insulin resistance in rodents. However, the relevance of resistin in human obesity and insulin resistance has been challenged by the difference between human and rodent resistin and the controversies in human epidemiologic studies. Instead, recent human clinical studies and experiments support the idea that human resistin is an inflammatory mediator and a biomarker of cardiovascular diseases, especially in atherosclerosis and heart failure. Thus, we focused on the recent evidence of the role of human resistin in cardiovascular disease.Key words: resistin, adipokine, inflammation, atherosclerosis, heart failure, cardiovascular disease Resistin as an adipokine in rodent modelPrevalence of obesity is growing rapidly and it has become a major worldwide health problem because it is strongly associated with a number of diseases, including insulin resistance, type 2 diabetes, atherosclerosis and ischemic heart disease, that reduce life expectancy and together have huge economic and societal consequences (Ouchi et al., 2011). Adipocytes or adipose tissue have been considered to hold responsibility for development of such obesity-related disorders and became the target of tremendous studies to elucidate the mechanism of obesity-related disorders and the clues to cure or prevent those problems. These studies have identified adipocytes or adipose tissue, which were previously well-known for their essential role as energy storage depots, as an active endocrine gland that secretes important hormones, cytokines, vasoactive substances, and other peptides. Adipocytes or adipose tissue, thereby, influence local adipocyte biology as well as systemic metabolism at sites as diverse as brain, liver, muscle, B cells, gonads, lymphoid organs, and systemic vasculature as a regulator of food intake and nutrient metabolism, insulin sensitivity, stress responses, reproduction, bone growth, and S.e. Lee, et al. 28 inflammation (Kahn and Flier, 2000). These factors that are expressed and secreted by adipocytes or adipose tissue are collectively referred to as adipokines. A growing number of proteins have been identified as an adipokines since adipsin was identified as an adipokine by Cook et al. (1987) and TNFalpha by Hotamisligil et al. (1993). Subsequently leptin was identified to be secreted by adipose tissue and to regulate food intake and energy expenditure in an endocrine manner by Zhang et al. (1994). Adiponectin was discovered as an adipokine that is decreased in obesity by Scherer et al. (1995), Hu et al. (1996) and Maeda et al. (1996), and many succeeding studies showed that it has protective role against several metabolic and cardiovascular disorders associated with obesity. It has been widely recognized that the abnormal expression of these factors strongly contributes the pathogenic processes of obesity related disorders (Ouchi et al., 2011). Thus much attention has been paid to discovering new factors secreted by adipose tissue ...

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“…In contrast, several other studies (29,30) found that resistin levels are higher in different cardiovascular conditions. More important, the same Pilz et al (28) found an increase in mortality in hyperresistinemic patients, and Lubos et al (31) demonstrated that resistin levels predict cardiovascular mortality in patients with coronary artery disease. Our study found a mechanism through which resistin can affect cardiovascular physiology and contribute to human disease, thus extending recent observations (32) showing that vascular cells are a target of resistin also independently of metabolic effects.…”

Section: Discussionmentioning

confidence: 92%

“…On this note, epidemiological studies so far have been inconclusive. A recent study (27) did not find an association between resistin levels and cardiovascular events in Korean diabetic patients, and Pilz et al (28) related resistin levels to inflammatory processes and renal function but not to the incidence of some cardiovascular diseases. In contrast, several other studies (29,30) found that resistin levels are higher in different cardiovascular conditions.…”

Section: Discussionmentioning

confidence: 99%

Resistin Impairs Insulin-Evoked Vasodilation

et al. 2008

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OBJECTIVE-Since vascular dysfunction is a main trait of obese subjects, in the present study we evaluated the vascular impact of resistin, a recently discovered hormone markedly increased in obesity.RESEARCH DESIGN AND METHODS-We performed our analysis on aortic and mesenteric segments from young and old C57BL/6 mice and on cultured endothelial cells. Resistin-induced vascular effect was evaluated in vitro and in vivo. Molecular analyses were performed by immunoprecipitation and Western blotting.RESULTS-Recombinant murine resistin did not induce changes in either basal vascular tone or phenylephrine-induced vascular contraction. In contrast, both in vivo and in vitro administration of resistin significantly impaired dose-dependent insulin-evoked vasodilation by reducing endothelial nitric oxide synthase (eNOS) enzymatic activity. This effect of resistin was selective for insulin vascular action, since vasodilatation induced by increasing doses of acetylcholine or nitroglycerin was not influenced by the hormone. Molecular analysis of endothelial cells further detailed resistin-induced vascular resistance by showing impairment of insulin-evoked AKT and eNOS phosphorylations after exposure to resistin. Even this latter abnormality is selective of insulin signaling since AKT/eNOS phosphorylations are normally activated during acetylcholine stimulation. More important, the resistin-induced endothelial dysfunction depends on resistin's ability to alter insulin receptor substrate (IRS)-1 tyrosine/serine phosphorylation and its consequent interaction with phosphatidylinositol 3-kinase.CONCLUSIONS-Our results demonstrate that resistin is able to induce a selective vascular insulin resistance-impairing endothelial IRS-1 signaling pathway that leads to eNOS activation and vasodilation. Diabetes 57:577-583, 2008

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Implications of resistin plasma levels in subjects undergoing coronary angiography

Cited by 43 publications

References 38 publications

Adipose tissue and vascular inflammation in coronary artery disease

Adipose tissue and vascular inflammation in coronary artery disease

Human resistin in cardiovascular disease

Resistin Impairs Insulin-Evoked Vasodilation

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