Preliminary experience with resistin assessment in common population.

Stejskal, David; Proskova, Jitka; Juráková, Renata; Bártek, J

doi:10.5507/bp.2002.009

Cited by 21 publications

(12 citation statements)

References 11 publications

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“…No correlation was proved between resistin and age, sex or BMI. The values of resistin in healthy probands under the present study (Group C) did not differ from those recorded previously 18 . With regard to the fact that a correlation was found between the concentrations of resistin and leptin in healthy probands (which we did not find in diabetics and persons with severe systemic inflammation), we assume that in healthy individuals there exists a metabolic regulation in which both factors are involved 14 .…”

Section: Pathophysiology Of Resistin -Human Studycontrasting

confidence: 46%

Resistin - concentrations in persons with type 2 diabetes mellitus and in individuals with acute inflammatory disease

Stejskal¹,

Bártek²,

Juráková³

et al. 2003

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Resistin is a recently discovered signal molecule, which could help elucidation of the pathophysiology of the insulin resistance and its correlation with obesity. As little information was available about resistin determination in venous blood at the time of our study, we focused on the question whether any correlation exists between persons with type 2 diabetes mellitus, with systemic inflammation, healthy persons and resistin concentrations and laboratory markers of inflammation, peptone, BMI. Differences of resistin values in these types of volunteers were studied as well.Methods: Persons under study were divided into 3 groups: group A -with clinical signs of inflammatory disease of respiratory tract, leukocytosis > 10000/ul and CRP concentration > 50 mg/l (n = 35); group B -with well controlled type 2 DM treated by oral antidiabetic drugs, without clinical signs of inflammation and negative case history of acute disease (n = 12); group C -without clinical signs of inflammation and negative case history of acute disease (n = 77). For all volunteers we determined BMI index and examined resistin, leptin, interleukin 6, TNF-alpha, Na, K, Cl, insulin, cholesterol, HDL-cholesterol, LDL-cholesterol, triacylglycerols, creatinine, uric acid, ALT, AST, GMT, P, Mg and albumin in serum.Results: Persons with clinical signs of severe inflammation had higher concentrations of Il6, CRP, resistin and a markedly lower BMI, decreased values of glucose, sodium, triacylglycerols, cholesterol, LDL-cholesterol and HDL-cholesterol compared to diabetics of type 2 (p < 0.05). Persons with clinical signs of severe inflammation showed significantly higher concentrations of TNF-alpha, Il6, CRP, resistin, glucose, leptin and considerably lower values of albumin, sodium and HDL-cholesterol than healthy individuals (p < 0.05). Persons with type 2 DM had markedly higher values of BMI, CRP, glucose, triacylglycerols, LDL-cholesterol, GMT and leptin, compared to healthy volunteers (p < 0.05). None of the three groups differed markedly in age or sex.Healthy volunteers show a significant correlation between leptin and resistin (correlation coefficient 0.82); this correlation was not found in patients with inflammation and type 2 DM. The group of volunteers with inflammations was found to have a significant positive correlation between resistin and inflammatory markers (correlation coefficient 0.3-0.5), negative correlation between resistin and cholesterol. We also found positive correlations between leptin and BMI as well as negative correlations between leptin and CRP. No significant correlations between resistin and other studied parameters were found in persons with type 2 DM.Conclusion: In healthy population a correlation was found between leptin and resistin concentrations in serum. In patients with severe inflammatory disease a correlation between resistin concentration and laboratory markers of inflammation was shown, however, no correlation was found between leptin and resistin. Resistin concentration in the serum of these patients is s...

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Section: Pathophysiology Of Resistin -Human Studycontrasting

confidence: 46%

Resistin - concentrations in persons with type 2 diabetes mellitus and in individuals with acute inflammatory disease

Stejskal¹,

Bártek²,

Juráková³

et al. 2003

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Preliminary observations suggest that mean plasma levels in patients with diabetes are Ϸ40 ng/mL. 8,9 The present study reports for the first time the direct vasoactive effects of human recombinant resistin in cultured endothelial cells. Resistin-treated endothelial cells responded by greater production of ET-1 and augmented ET-1 mRNA expression.…”

Section: Discussionmentioning

confidence: 91%

“…The plasma concentrations of resistin in patients with insulin resistance remain to be carefully defined, although preliminary studies suggest that mean circulating resistin levels may be Ϸ40 ng/mL in diabetes (versus Ϸ15 ng/mL in lean nondiabetic patients). 8,9 Cell Adhesion Molecule Expression Endothelial cells were detached by nonenzymatic cell dissociation solution (Sigma) and were stained for CD106 (VCAM-1) or CD31 (platelet-endothelial cell adhesion molecule-1, or PECAM-1) with monoclonal R-phycoerythrin-conjugated anti-human CD106 or anti-CD31 antibodies (Pharmingen), all at a 1:5 dilution. Cells were analyzed with a Beckman Coulter EPICS XL flow cytometer with EXPO32 ADC software.…”

Section: Cell Culturementioning

confidence: 99%

Resistin Promotes Endothelial Cell Activation

et al. 2003

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Background-Adipocyte-derived hormones may represent a mechanism linking insulin resistance to cardiovascular disease. In the present study, we evaluated the direct effects of resistin, a novel adipocyte-derived hormone, on endothelial activation. Methods and Results-Endothelial cells (ECs) were incubated with human recombinant resistin (10 to 100 ng/ML, 24 hours), and endothelin-1 (ET-1) release, ET-1 mRNA expression, and nitric oxide (NO) production were assessed. Transient transfection assays were used to evaluate the effects of resistin on transcription of human ET-1 gene promoter. Furthermore, the effects of resistin on AP-1-mutated ET-1 promoter were evaluated. The effects of resistin on expression of vascular cell adhesion molecule (VCAM-1) and monocyte chemoattractant chemokine (MCP-1) were studied in addition to CD40 receptor, CD40 ligand-induced MCP-1 expression, and tumor necrosis factor receptorassociated factor-3 (TRAF3), an inhibitor of CD40 signaling. Incubation of ECs with resistin resulted in an increase in ET-1 release and ET-1 mRNA expression, with no change in NO production. Whereas treatment with resistin resulted in an increase in ET-1 promoter activity, the AP-1-mutated promoter was inactive after resistin stimulation. Additionally, resistin-treated cells showed increased expression of VCAM-1 and MCP-1, with concomitant reductions in TRAF-3 expression. Resistin did not alter CD40 receptor expression; however, increased CD40 ligand induced MCP-1 production. Conclusions-The novel adipokine resistin exerts direct effects to promote EC activation by promoting ET-1 release, in part by inducing ET-1 promoter activity via the AP-1 site. Furthermore, resistin upregulates adhesion molecules and chemokines and downregulates TRAF-3, an inhibitor of CD40 ligand signaling. In this fashion, resistin may be mechanistically linked to cardiovascular disease in the metabolic syndrome.

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“…17 The plasma concentrations of resistin in patients with insulin resistance remain to be carefully defined, although preliminary studies suggest that mean circulating resistin levels may be 40 ng/mL in diabetes (versus 15 ng/mL in lean nondiabetic patients). 27,28 In the study of Shalev et al, 29 the average serum resistin level in healthy control subjects was 30.7 ng/mL, and serum resistin levels were significantly elevated in patients with diabetes (49.7 ng/mL). The differences in these results may also be due to different ELISAs used in different studies.…”

Section: Discussionmentioning

confidence: 99%

Resistin Promotes Smooth Muscle Cell Proliferation Through Activation of Extracellular Signal–Regulated Kinase 1/2 and Phosphatidylinositol 3-Kinase Pathways

et al. 2004

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Background-Resistin, a novel adipokine, is elevated in patients with type 2 diabetes and may play a role in the vascular complications of this disorder. One recent study has shown that resistin has a proinflammatory effect on endothelial cells. However, there is no information on whether resistin could also affect vascular smooth muscle cells (SMCs). Thus, the purpose of this study was to assess whether resistin could induce SMC proliferation and to study the mechanisms whereby resistin signals in SMCs. Methods and Results-Human aortic smooth muscle cells (HASMCs) were stimulated with increasing concentrations of resistin for 48 hours. Cell proliferation was induced by resistin in a dose-dependent manner as assessed by direct cell counting. To gain more insights into the mechanism of action of resistin, we investigated the extracellular signal-regulated kinase (ERK) and/or phosphatidylinositol 3-kinase (PI3K) signaling pathways. Transient phosphorylation of the p42/44 mitogen-activated protein kinase (ERK 1/2) occurred after addition of resistin to HASMCs. U0126, a specific inhibitor of ERK phosphorylation, significantly inhibited ERK 1/2 phosphorylation and reduced resistinsimulated proliferation of HASMCs. LY294002, a specific PI3K inhibitor, also significantly inhibited HASMC proliferation after resistin stimulation. Conclusions-Our results demonstrate that resistin induces HASMC proliferation through both ERK 1/2 and Akt signaling pathways. The proliferative action exerted by resistin on HASMCs may account in part for the increased incidence of restenosis in diabetes patients.

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Preliminary experience with resistin assessment in common population.

Cited by 21 publications

References 11 publications

Resistin - concentrations in persons with type 2 diabetes mellitus and in individuals with acute inflammatory disease

Resistin - concentrations in persons with type 2 diabetes mellitus and in individuals with acute inflammatory disease

Resistin Promotes Endothelial Cell Activation

Resistin Promotes Smooth Muscle Cell Proliferation Through Activation of Extracellular Signal–Regulated Kinase 1/2 and Phosphatidylinositol 3-Kinase Pathways

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