Resistin is linked to inflammation, and leptin to metabolic syndrome, in women with inflammatory arthritis

Kontunen, Perttu; Vuolteenaho, Katriina; Nieminen, Riina; Lehtimäki, Lauri; Kautiainen, Hannu; Kesäniemi, Y. Antero; Ukkola, Olavi; Kauppi, Markku; Hakala, M; Moilanen, Eeva

doi:10.3109/03009742.2010.548827

Cited by 24 publications

(28 citation statements)

References 46 publications

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“…Records after duplicates removed (n = 31) [22] showed that leptin levels were increased only in patients with RA and concomitant diagnosis of metabolic syndrome (MetS). Kang et al (2013) [23] demonstrated that TNF-α was positively associated to leptin and the latter was associated with various metabolic risk factors, including insulin resistance.…”

Section: Leptinmentioning

confidence: 99%

“…The authors found that the level of resistin in serum did not differ between patients and controls, but observed that serum resistin were positively associated with CRP levels in RA patients, suggesting a pro inflammatory action of this cytokine. Kontunen et al (2011) [22] reported that high levels of resistin are associated with RA, regardless of the presence of MetS. Fadda et al (2013) [37] compared resistin levels in serum and synovial fluid of patients with RA and osteoarthritis and found higher levels in patients with RA.…”

Section: Resistinmentioning

confidence: 99%

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Adipokines in rheumatoid arthritis

et al. 2018

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Rheumatoid arthritis affects millions of people worldwide and is considered a chronic multisystem disease whose causes are unknown. In general, the main objective of rheumatoid arthritis treatment is to improve the quality of life of patients by relieving pain, maintaining or improving functional capacity, preventing thus, disability. In recent years the role of adipokines in the pathogenesis of rheumatoid arthritis has been discussed but results are still conflicting. Although results from some studies have shown the implications of adipokines in the pathophysiology of autoimmune diseases, including rheumatoid arthritis, their role in the pathogenesis of disease progression is not clear. Thus, this review aimed to describe the association of key adipokines (leptin, resistin, visfatin and adiponectin) and rheumatoid arthritis, given the high prevalence of this disease and the important social impact caused by this chronic disabling disease.

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Section: Leptinmentioning

confidence: 99%

Section: Resistinmentioning

confidence: 99%

Adipokines in rheumatoid arthritis

et al. 2018

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“…Kontunen et al assessed leptin levels in patients with arthritis and MetS. Their results showed higher leptin levels in subjects with arthritis and MetS than arthritis patients without MetS [56]. This suggests that leptin is associated with MetS but not directly with arthritis, although a marked increase in plasma levels of leptin in patients with RA was noted [57].…”

Section: Leptinmentioning

confidence: 99%

“…In other study, Kontunen et al assessed adiponectin levels in patients with arthritis and MetS. Their results showed lower adiponectin levels in subjects with arthritis and MetS than arthritis patients without MetS [56]. Furthermore, Gonzalez-Gay et al suggested that low circulating adiponectin levels may be implicated in the development of CVD associated with RA.…”

Section: Adiponectinmentioning

confidence: 99%

Adipokines, Metabolic Syndrome and Rheumatic Diseases

Abella

Scotece

Conde

et al. 2014

Journal of Immunology Research

137

113

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The metabolic syndrome (MetS) is a cluster of cardiometabolic disorders that result from the increasing prevalence of obesity. The major components of MetS include insulin resistance, central obesity, dyslipidemia, and hypertension. MetS identifies the central obesity with increased risk for cardiovascular diseases (CVDs) and type-2 diabetes mellitus (T2DM). Patients with rheumatic diseases, such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, and ankylosing spondylitis, have increased prevalence of CVDs. Moreover, CVD risk is increased when obesity is present in these patients. However, traditional cardiovascular risk factors do not completely explain the enhanced cardiovascular risk in this population. Thus, MetS and the altered secretion patterns of proinflammatory adipokines present in obesity could be the link between CVDs and rheumatic diseases. Furthermore, adipokines have been linked to the pathogenesis of MetS and its comorbidities through their effects on vascular function and inflammation. In the present paper, we review recent evidence of the role played by adipokines in the modulation of MetS in the general population, and in patients with rheumatic diseases.

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“…As many studies have already suggested, PPARs might be an important link between these two complex systems, and as shown in the present study, PPAR agonists have anti-inflammatory properties in classical inflammatory models. It has been shown that a good treatment of metabolic diseases reduces the low-grade inflammation associated with obesity [38]. But could the modification of metabolic pathways reduce the inflammatory responses associated to classical inflammatory diseases?…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory properties of a dual PPARgamma/alpha agonist muraglitazar in in vitro and in vivo models

et al. 2013

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IntroductionPeroxisome proliferator-activated receptor (PPAR) agonists are widely used drugs in the treatment of diabetes and dyslipidemia. In addition to their metabolic effects, PPAR isoforms PPARα and PPARγ are also involved in the regulation of immune responses and inflammation. In the present study, we investigated the effects of a dual PPARγ/α agonist muraglitazar on inflammatory gene expression in activated macrophages and on carrageenan-induced inflammation in the mouse.MethodsJ774 murine macrophages were activated by lipopolysaccharide (LPS) and treated with dual PPARγ/α agonist muraglitazar, PPARγ agonist GW1929 or PPARα agonist fenofibrate. The effects of PPAR agonists on cytokine production and the activation of inducible nitric oxide synthase (iNOS) pathway were investigated by ELISA, Griess method, Western blotting and quantitative RT-PCR. Nuclear translocation, DNA-binding activity and reporter gene assays were used to assess the activity of nuclear factor kappa B (NF-kB) transcription factor. Carrageenan-induced paw oedema was used as an in vivo model of acute inflammation.ResultsMuraglitazar as well as PPARγ agonist GW1929 and PPARα agonist fenofibrate inhibited LPS-induced iNOS expression and NO production in activated macrophages in a dose-dependent manner. Inhibition of iNOS expression by muraglitazar included both transcriptional and post-transcriptional components; the former being shared by GW1929 and the latter by fenofibrate. All tested PPAR agonists also inhibited IL-6 production, while TNFα production was reduced by muraglitazar and GW1929, but not by fenofibrate. Interestingly, the anti-inflammatory properties of muraglitazar were also translated in vivo. This was evidenced by the finding that muraglitazar inhibited carrageenan-induced paw inflammation in a dose-dependent manner in mice as did iNOS inhibitor L-NIL and anti-inflammatory steroid dexamethasone.ConclusionsThese results show that muraglitazar has anti-inflammatory properties both in vitro and in vivo and these effects reflect the agonistic action through both PPARα and PPARγ.

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Resistin is linked to inflammation, and leptin to metabolic syndrome, in women with inflammatory arthritis

Abstract: The results show that high resistin levels are associated with arthritis independently of MetS, whereas leptin is increased only in arthritis patients with MetS.

Cited by 24 publications

References 46 publications

Adipokines in rheumatoid arthritis

Adipokines in rheumatoid arthritis

Adipokines, Metabolic Syndrome and Rheumatic Diseases

Anti-inflammatory properties of a dual PPARgamma/alpha agonist muraglitazar in in vitro and in vivo models

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