Resistin Is an Inflammatory Marker of Atherosclerosis in Humans

Reilly, Muredach P.; Lehrke, Michael; Wolfe, Megan L.; Rohatgi, Anand; Lazar, Mitchell A.; Rader, Daniel J.

doi:10.1161/01.cir.0000155620.10387.43

Cited by 796 publications

(709 citation statements)

References 58 publications

(71 reference statements)

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“…A growing amount of data support the interrelationship of eGFR with inflammatory involvement as well as a distinct role of low-grade inflammation in the progression of chronic kidney disease 3,9,14,15 and diffuse atherosclerosis reflected by microalbuminuria. 25,26 In these lines, although resistin mediates diverse biological effects of cytokines, [27][28][29] there was a lack of association between resistin and white blood cell count in our population, a finding that is in contrast with previous reports. 6,28 It should be noted that other more sensitive markers of subclinical inflammation such as C-reactive protein were not estimated in this study, thus the link between hyperresistinemia and inflammation may be missed.…”

Section: Discussioncontrasting

confidence: 99%

Independent association of circulating resistin with glomerular filtration rate in the early stages of essential hypertension

et al. 2009

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Resistin, a newly discovered protein, promotes endothelial dysfunction and proinflammatory activation, contributing to subclinical atherosclerosis in different clinical settings. In this study we sought to investigate the relationship of increased resistin levels with estimated glomerular filtration rate (eGFR), the most established marker of kidney impairment, in hypertensive subjects. Our population consisted of 132 untreated non-diabetic subjects with stage I-II essential hypertension (49 males, mean age ¼ 54 years, office blood pressure (BP) ¼ 159/100 mm Hg). In all patients eGFR was assessed by the Modification in Renal Disease equation and venous blood sampling was performed for estimation of resistin concentrations. The distribution of resistin was split by the median (4.63 ng ml À1 ) and accordingly subjects were stratified into those with high and low values. Hypertensive patients with high (n ¼ 66) compared to those with low resistin (n ¼ 66) exhibited lower eGFR values (77.1±9.4 vs 89.1±12.2 ml min À1 per 1.73m 2 , Po0.0001), even after adjustment for established confounders. In the total population, resistin was associated with 24-h systolic BP (r ¼ 0.244, Po0.05), serum creatinine (r ¼ 0.311, P ¼ 0.007) and eGFR (r ¼ À0.519, Po0.0001). Multiple regression analysis revealed that age (b ¼ 0.379, P ¼ 0.01), body mass index (b ¼ 0.158, P ¼ 0.022), 24-h systolic BP (b ¼ 0.284, P ¼ 0.006) and resistin (b ¼ 0.429, Po0.0001) were independent predictors of eGFR (R 2 ¼ 0.436, Po0.0001). In essential hypertensive subjects, higher resistin levels are associated with renal function impairment, as reflected by decreased eGFR. Moreover, the independent association of resistin with eGFR suggests involvement of resistin in the progression of kidney damage in the early stages of hypertension.

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Section: Discussioncontrasting

confidence: 99%

Independent association of circulating resistin with glomerular filtration rate in the early stages of essential hypertension

et al. 2009

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“…38 Available data also support a role of r in determining an increase of inflammation and atherosclerosis. 39 The positive effect of losartan in reducing r had already been observed in an experimental model of acute hyperinsulinemia in healthy humans. 40 However, to the best of our knowledge, no other study, except ours, has evaluated the effects of either losartan or ramipril on such a large spectrum of adipokines.…”

Section: Correlationsmentioning

confidence: 88%

Different actions of losartan and ramipril on adipose tissue activity and vascular remodeling biomarkers in hypertensive patients

et al. 2010

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We planned a randomized, double blind clinical trial to evaluate whether an antihypertensive intervention at the proximal or distal level of the renin-angiotensin-aldosterone system could have different effects on a broad range of innovative cardiovascular risk biomarkers. A total of 288 hypertensive Caucasian patients (115 men and 113 women), aged X18 years, were enrolled in this study. They were randomized to take losartan 50 mg per day or ramipril 5 mg per day for 1 month and titrated up to 100 mg per day and 10 mg per day for 13 months, respectively. At baseline, 1, 2 and 14 months after therapy initiation, we evaluated the following parameters: body weight, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting plasma glucose (FPG), M-value, adiponectin (ADN), resistin (r), retinol binding protein-4 (RBP-4), visfatin, vaspin, high-sensitivity C-reactive protein (Hs-CRP), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9). No variation of body weight, BMI, FPG or vaspin was obtained with either treatment. We recorded a similar improvement in SBP, DBP and Hs-CRP with both treatments; however, losartan also increased M-value, ADN and visfatin, whereas ramipril did not. Furthermore, losartan decreased r, RBP-4, MMP-2 and MMP-9, whereas ramipril did not have any effect on these parameters. In conclusion, we observed that short-term treatment with losartan improved several metabolic parameters (M-value, ADN, RBP-4, r and visfatin) and decreased vascular remodeling biomarkers (MMP-2 and MMP-9) in hypertensive subjects, whereas ramipril did not.

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“…We tested whether in the athletes an increased serum resistin concentration reflected ongoing pro-inflammatory events. In fact, resistin's structure is similar to that of proteins involved in inflammatory processes and its serum concentration was found to be associated with coronary artery calcification independently of the C-reactive protein and other inflammatory markers [17]. In addition, exercise activity is known to induce acutely increments of the circulating levels of many pro-and anti-inflammatory cytokines and chemokines [31].…”

Section: Discussionmentioning

confidence: 99%

“…In fact, studies in humans reported conflicting results, indicating decreased or increased resistin levels in obesity, opposite responses to insulin-sensitisers and contradictory correlations between resistin and markers of insulin resistance [8][9][10][11][12][13][14][15]. It has also been suggested that resistin plays a role in inflammatory conditions, because it is expressed in human macrophages [16] and because recent data have supported the existence of an independent association of resistin with the inflammatory factors IL-6 and C-reactive protein [17]. The aim of the present study was to examine whether resistin is a marker of insulin resistance or lowgrade inflammation in a human model of extreme insulin sensitivity, i.e.…”

Section: Introductionmentioning

confidence: 99%

Increased serum resistin in elite endurance athletes with high insulin sensitivity

et al. 2006

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Aims/hypothesis: Resistin is an adipokine associated with obesity and type 2 diabetes in animal models, but in humans its role remains uncertain. This study was undertaken to test whether serum resistin is related to insulin resistance and markers of low-grade inflammation in elite athletes taken as a model of extreme insulin sensitivity. Subjects materials and methods: In 23 elite athletes (sprinters, middle-distance and marathon runners) and in 72 sedentary men including lean and obese individuals with NGT, and obese individuals with IGT or new-onset type 2 diabetes, we assessed insulin sensitivity using a whole-body insulin-sensitivity index (WBISI) derived from a 3-h OGTT; energy homeostasis was also assessed by means of indirect calorimetry, along with circulating adipokines and low-grade pro-inflammatory cyto-chemokines.Results: Professional athletes had increased WBISIs (p<0.001) and lipid oxidation (p<0.03); they also showed higher serum resistin concentrations (p<0.001), although the pro-inflammatory chemokines were not increased in comparison with the other study groups. Resistin was independently associated only with fasting plasma NEFA. Increased resistin was detected in the middle-distance and marathon runners, but not in the sprinters when compared with the lean, young, sedentary individuals. Conclusions/interpretation: Serum resistin concentration is increased in elite athletes, providing evidence against the notion that resistin levels reflect insulin resistance in humans, as seen in animal studies. Increased resistin was observed in aerobicendurance, but not sustained-power athletes and this feature appeared to be independently associated with parameters of fatty acid metabolism.

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Resistin Is an Inflammatory Marker of Atherosclerosis in Humans

Cited by 796 publications

References 58 publications

Independent association of circulating resistin with glomerular filtration rate in the early stages of essential hypertension

Independent association of circulating resistin with glomerular filtration rate in the early stages of essential hypertension

Different actions of losartan and ramipril on adipose tissue activity and vascular remodeling biomarkers in hypertensive patients

Increased serum resistin in elite endurance athletes with high insulin sensitivity

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