Resistin increases platelet P-selectin levels via p38 MAPK signal pathway

Qiu, Wenbing; Chen, Naping; Zhang, Qin; Zhuo, Liyuan; Wang, Xihong; Wang, Dongming; Jin, Hong

doi:10.1177/1479164113513912

Cited by 23 publications

(11 citation statements)

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“…Human resistin also increases the proliferation and migration of human endothelial cells and vascular smooth muscle cells (VSMC) and increases endothelial permeability, which promotes endothelial cell/monocyte adhesion and infiltration [22]; these actions are mediated by the ERK and p38 mitogen-activated protein kinase signaling pathways [20]. Furthermore, resistin inhibits endothelial nitric oxide synthase via oxidative stress in human endothelial cells [23], promotes foam cell formation in human macrophages, induces a prothrombotic phenotype in human endothelial cells [17], and induces platelet activation by increasing P-selectin expression [24]. Taken together, these findings suggest that human resistin might play an important regulatory role in the modulation of interactions between endothelial cells, monocytes/macrophages, and VSMC in the pathogenesis and progression of atherosclerosis [25].…”

Section: Role Of Human Resistin In Atherosclerosismentioning

confidence: 99%

Linking resistin, inflammation, and cardiometabolic diseases

Park

Kwak

Kim

et al. 2017

Korean J Intern Med

178

150

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Adipose tissue secretes a variety of bioactive substances that are associated with chronic inflammation, insulin resistance, and an increased risk of type 2 diabetes mellitus. While resistin was first known as an adipocyte-secreted hormone (adipokine) linked to obesity and insulin resistance in rodents, it is predominantly expressed and secreted by macrophages in humans. Epidemiological and genetic studies indicate that increased resistin levels are associated with the development of insulin resistance, diabetes, and cardiovascular disease. Resistin also appears to mediate the pathogenesis of atherosclerosis by promoting endothelial dysfunction, vascular smooth muscle cell proliferation, arterial inflammation, and the formation of foam cells. Thus, resistin is predictive of atherosclerosis and poor clinical outcomes in patients with cardiovascular disease and heart failure. Furthermore, recent evidence suggests that resistin is associated with atherogenic dyslipidemia and hypertension. The present review will focus on the role of human resistin in the pathogeneses of inflammation and obesity-related diseases.

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Section: Role Of Human Resistin In Atherosclerosismentioning

confidence: 99%

Linking resistin, inflammation, and cardiometabolic diseases

Park

Kwak

Kim

et al. 2017

Korean J Intern Med

178

150

View full text Add to dashboard Cite

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“…Epidemiological cross-sectional associations can offer only speculation about the biology underlying them. On one hand we can speculate that, through its pro-inflammatory effect [ 27 , 28 ], resistin may well be deleterious on kidney function, quite similarly to what is believed for cardiovascular disease [ 19 , 29 , 30 ]. On the other hand, although we have previously shown that serum resistin is inversely associated with eGFR also in relatively young, non diabetic subjects with normal kidney function [ 17 ], we cannot exclude that high resistin is simply a consequence of reduced glomerular filtration rate, a hallmark of aged diabetic patients as those we here studied.…”

Section: Discussionmentioning

confidence: 99%

Serum Resistin and Glomerular Filtration Rate in Patients with Type 2 Diabetes

et al. 2015

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BackgroundHigh serum levels of the pro-inflammatory adipokine resistin have been associated with decreased renal function in the general population. The goal of this study was to investigate whether such association is also present among diabetic subjects, who are at increased risk of renal function loss.MethodsThe cross-sectional association between serum resistin levels and estimated glomerular filtration rate (eGFR) was investigated in 1,560 type 2 diabetic (T2D) patients of European ancestry comprised in two different cohorts: 762 patients from San Giovanni Rotondo (SGR; Italy) and 798 patients from Boston (US).ResultsSerum resistin was inversely associated with eGFR in SGR [β (SE) for one SD of resistin increment = -1.01 (0.70) ml/min/1.73m2, p = 0.019] and in Boston [β (SE) = -5.31 (0.74) ml/min/1.73m2, p < 0.001] samples, as well as in the two studies combined [β (SE) = -3.42 (0.52) ml/min/1.73m2, p < 0.001]. The association was unaffected by adjustment for smoking habits, BMI, waist circumference, diabetes duration, HbA1c, insulin treatment, hypertension and lipid-lowering therapy: β (SE) for one SD of resistin increment = -1.07 (0.70), p = 0.02; -5.50 (0.88), p < 0.001; and -2.81 (0.55) ml/min/1.73m2, p < .001, in SGR, Boston and the two studies combined, respectively. The association was significantly stronger in men than in women (p for resistin-by-gender interaction = 0.003). For each resistin SD increment, the odds of having eGFR < 0 ml/min/1.73m2 increased by 22% (OR = 1.22; 95% CI 1.02–1.44; p = 0.025) in SGR sample, 69% (OR = 1.69; 95% CI 1.38–2.07; p < 0.001) in Boston sample, and 47% (OR = 1.47; 95% CI 1.29–1.68; p < 0.001) in the two studies considered together. Similar associations were observed in the adjusted model: OR 95% CI for each SD resistin increment being 1.23 (1.03–1.46), p = 0.021; 1.52 (1.20–1.92), p < 0.001; 1.33 (1.16–1.53), p < 0.001, in SGR, Boston and the two studies combined, respectively.ConclusionsThis is the first report of an association between high serum resistin and low eGFR in patients with T2D of European ancestry.

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“…This issue is noteworthy that; resistin in addition to adipose tissue is produced in blood mononuclear cells and leukocytes in human body [11,49]. It is likely; these cells play a role for increasing resistin gene expression in response to exercise stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to adipose tissue, high levels of resistin exist in monocytes, macrophages, and spleen and bone marrow cells [11]. Several studies have been shown that, resistin plays a role in the development of insulin resistance (IR) [10,12,13].…”

Section: Introductionmentioning

confidence: 99%

Blood Levels of Resistin, Glycemic Indices and Lipid Profile in Women with Type 2 Diabetes

Tofighi¹,

Samadian²,

Mahdizadeh³

2016

J Diabetes Metab

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We aimed to compare the changes in PRL with glycemic indices and lipid profile and also to investigate the relationship of insulin resistance (IR) with PRL in obese postmenopausal women with diabetes mellitus type 2 (DMT2) following 12-week aerobic, resistance and combined exercises, while our inclusion and exclusion criteria and also design exercise protocol differ from other studies in this field. In a quasi-experimental study for 12 weeks, 40 women with DMT2 were randomly selected by availability and purposive sampling and divided into four equal groups of aerobic training, resistance, combined and control group. Aerobic group accomplished aerobic exercise (AEX), 3x/week, for 20-50 minutes at 50-70% of maximum heart rate. Resistance group received resistance exercise (REX), 3x/week in three sets of 10 repetitions with 40-60% of one repetition maximum. The program in combined group consisted of a combination of AEX and REX with the same intensity and duration (included 2 sessions of AEX and 1 session of REX per week. But fortnightly, the numbers of these sessions were changed with each other). The control group was without exercise program. Blood samples for determination of PRL, lipid profile and glycemic indices in pre-and post-tests were collected. HOMA-IR equation was used to calculate insulin resistance. Statistical analysis was performed using SPSS software version 21. According to our finding; the effect of AEX and combined exercises was more than control group on the increasing PRL. The result of AEX in weight loss was more than REX however, the outcome of REX in insulin and IR reducing; also TC declining was more than the AEX. While the effect of combined group in decreasing body fat percent was more than AEX group, but the consequence of AEX was more than the combined group for reducing waist-to-hip ratio (WHR). The effect of the combined group in reducing low density lipoprotein (LDL) was more than the REX group. Also, weight, fasting blood glucose, insulin, triglycerides, LDL, glycosylated hemoglobin A1c and WHR were the predictors of IR. It seems that, during the study period, all three types of exercises through different mechanisms had valuable effects on glycemic indices and lipid profile in DMT2 patients. Also due to the increase in PRL and non-significant correlation with IR; it is doubtful that resistin be as a factor in the incidence of DMT2.

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Resistin increases platelet P-selectin levels via p38 MAPK signal pathway

Cited by 23 publications

References 11 publications

Linking resistin, inflammation, and cardiometabolic diseases

Linking resistin, inflammation, and cardiometabolic diseases

Serum Resistin and Glomerular Filtration Rate in Patients with Type 2 Diabetes

Blood Levels of Resistin, Glycemic Indices and Lipid Profile in Women with Type 2 Diabetes

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