Elevated Resistin Levels are Associated with Inflammation in Hemodialysis Patients with Failed Renal Allografts

Akagun, Tulin; Çalışkan, Yaşar; Yazıcı, Halil; Özkök, Abdullah; Telci, Ayşegül; Türkmen, Aydın; Yildiz, Alaattin; Sever, Mehmet Şükrü

doi:10.5301/ijao.5000319

Cited by 10 publications

(8 citation statements)

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“…Resistin is a novel adipocytokine that may play a role in the pathophysiology of insulin resistance and obesity [ 27 ]. Resistin is also known to increase inflammation by upregulating IL-6 and TNF-α levels [ 18 , 28 , 29 ]. In aggrement with these results, serum resistin levels were significantly associated with pro-inflammatory cytokines such as serum TNF-α and leptin levels in the present study.…”

Section: Discussionmentioning

confidence: 99%

CD133+ cells are associated with ADIPOCYTOKINES and endothelial dysfunction in hemodialysis patients

Özkök

Atas²,

Çınar

et al. 2017

BMC Nephrol

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BackgroundHemodialysis (HD) patients have increased risk of cardiovascular disease (CVD). Impaired stem cell health and adipocytokine metabolism may play important roles in the complex pathophysiological mechanisms of CVD in this patient population. We aimed to investigate the relationships between CD133+ cell counts, adipocytokines and parameters of endothelial dysfunction and atherosclerosis in HD patients.MethodsIn 58 chronic HD patients (male/female:28/30, mean age:58 ± 14 years), serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), leptin, adiponectin and resistin were measured by ELISA. Left ventricular mass index (LVMI), carotid intima-media thickness (CIMT), flow-mediated dilatation (FMD) of the brachial artery were measured. CD133+ cells were counted by flow cytometry (BD FACSCalibur-BD Bioscience,CA).ResultsCD133+ cell counts were inversely associated with FMD (r = −0.39, p = 0.007) and positively correlated with serum resistin (r = 0.45, p < 0.001) and serum TNF-α (r = 0.31, p = 0.02). Serum leptin levels were higher in high CD133 group compared to low CD133 group [32.37(12.74–72.29) vs 15.50(5.38–37.12)ng/mL, p = 0.03]. Serum leptin levels were correlated with TNF-α(r = 0.35, p = 0.009). Serum adiponectin levels were negatively correlated with serum leptin (r = −0.28, p = 0.03). Serum resistin levels were associated with TNF-α (r = 0.54, p < 0.001) and leptin (r = 0.29, p = 0.03). Serum IL-6 levels were significantly associated with LVMI (r = 0.31, p = 0.03). Serum IL-6 levels were significantly higher in patients with carotid plaque compared to patients without plaque [12.75(9.91–28.68) vs 8.27(5.97–14.04) pg/mL, p = 0.02]. In multiple linear regression analysis to determine the factors predicting LogFMD; dialysis vintage, LVMI and LogCD133+ cell counts were included as independent variables(R = 0.57, adjusted R-square = 0.27, p = 0.001). CD133+ cell count and LVMI were found to significantly predict FMD (p = 0.03 and p = 0.04 respectively).ConclusionCD133+ cells were associated with inflammation and endothelial dysfunction in HD patients. Serum leptin, resistin and TNF-α levels were positively related to CD133+ cell count. Impaired regulation of undifferentiated stem cells and adipocytokines might contribute to endothelial dysfunction in HD patients.

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Section: Discussionmentioning

confidence: 99%

CD133+ cells are associated with ADIPOCYTOKINES and endothelial dysfunction in hemodialysis patients

Özkök

Atas²,

Çınar

et al. 2017

BMC Nephrol

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“…More closely, increasing levels of resistin are correlated with an increase in pro-inflammatory cytokines, in particular in patients with metabolic syndrome [ 112 ]. Several studies have correlated increased resistin levels with increased hr-C-Reactive Protein (CRP) levels and TNF-α [ 32 , 111 , 113 , 114 ]. This suggests that increased resistin levels are associated with increased inflammation.…”

Section: Reviewmentioning

confidence: 99%

Human resistin and the RELM of Inflammation in diabesity

Hannan

Culligan

2015

Diabetol Metab Syndr

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The initial discovery of resistin and resistin-like molecules (RELMs) in rodents suggested a role for these adipocytokines in molecular linkage of obesity, Type 2 Diabetes mellitus and metabolic syndrome. Since then, it became apparent that the story of resistin and RELMs was very much of mice and men. The putative role of this adipokine family evolved from that of a conveyor of insulin resistance in rodents to instigator of inflammatory processes in humans. Structural dissimilarity, variance in distribution profiles and a lack of corroborating evidence for functional similarities separate the biological functions of resistin in humans from that of rodents. Although present in gross visceral fat deposits in humans, resistin is a component of inflammation, being released from infiltrating white blood cells of the sub-clinical chronic low grade inflammatory response accompanying obesity, rather than from the adipocyte itself. This led researchers to further explore the functions of the resistin family of proteins in inflammatory-related conditions such as atherosclerosis, as well as in cancers such as endometrial and gastric cancers. Although elevated levels of resistin have been found in these conditions, whether it is causative or as a result of these conditions still remains to be determined.

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“…However, whether the results obtained in mice are applicable to humans is still puzzling and controversial. ough some earlier publications questioned the link between resistin and insulin resistance in humans [see references [43][44][45][46][47][48] in (6)] our recent screening of the most recent 300 papers in PubMed under the term of resistin revealed 20 reports in which such an indirect link, evidenced by resistin levels in serum or tissues and various human pathologies such as adiposity, lung injury, metabolic syndrome, T2DM, gestational DM, diabetes-induced periodontitis, cardiovascular disease (CVD), non-alcoholic fatty liver disease (NFLD) and cancer was demonstrated (33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52).…”

Section: Comparative E Ects Of Resistin In Mice and Humansmentioning

confidence: 99%

Resistin activity in mice and humans affecting obesity, insulin resistance and T2DM: Blocking resistin action by resistin antagonis

Gertler

2014

Adipobiology

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Resistin, that was originally discovered in 2001 is named for its capacity to resist insulin action shown mainly in mice. However, there is a controversial history regarding its role in the pathogenesis of insulin resistance and type 2 diabetes mellitus (T2DM) in humans as most of the research was based on association between resistin blood levels and T2DM or other pathologies and so far the pharmacological e ect of recombinant resistin has not been tested in humans or even in primates. Resistin is a 12 kD cysteine-rich small protein acting as covalent dimer. Although human and mouse resistin genes and protein sequences share only approximately 60% homology, which is less than most hormones conserved across species, the genes are syntenic, with the mouse gene encoding resistin being located at a similar distance from the insulin receptor gene. Unlike mouse resistin which is mainly expressed in adipocytes, human resistin is synthesized predominantly in monocytes and macrophages, especially in the visceral adipose tissue. Resistin's e ects are mediated via paracrine and endocrine mechanisms of action through a receptor on the surface of target cells that remains controversial. Others and our study has shown that resistin interacts with the Toll-like receptor 4 (TLR4), however other putative receptors such as an isoform of decorin, mouse receptor tyrosine kinase-like orphan receptor 1 (ROR1) and adenylyl cyclase-associated protein 1 (CAP1) have been also proposed. Downstream targets of resistin provide indirect evidence for its function in intracellular pathways, involving impairment of insulin signaling, response to in ammation and proliferation. Despite the lack of in vivo data concerning the resistin receptor and signaling in primates or humans, there is a need to explore the in ammatory, metabolic and oncogenic e ects of resistin on human diseases. To address this challenge we have recently developed resistin mutant (C6A), acting as resistin antagonist which in several in vitro bioassays inhibited resistin action and in mice fed high fat diet (HFD) reduced weight, visceral fat, restored insulin sensitivity and attenuated HFD-induced neuroin amation. 2014; 6: 5-14 Adipobiology

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Elevated Resistin Levels are Associated with Inflammation in Hemodialysis Patients with Failed Renal Allografts

Abstract: Serum resistin levels are increased in HD patients with failed renal allografts very probably reflecting an allograft-induced chronic inflammatory state.

Cited by 10 publications

References 20 publications

CD133+ cells are associated with ADIPOCYTOKINES and endothelial dysfunction in hemodialysis patients

CD133+ cells are associated with ADIPOCYTOKINES and endothelial dysfunction in hemodialysis patients

Human resistin and the RELM of Inflammation in diabesity

Resistin activity in mice and humans affecting obesity, insulin resistance and T2DM: Blocking resistin action by resistin antagonis

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