Visfatin: A Putative Biomarker for Metabolic Syndrome is not Influenced by Pioglitazone or Simvastatin Treatment in Nondiabetic Patients at Cardiovascular Risk - Results from the PIOSTAT Study
Abstract:Insulin resistance and/or cardiovascular risk indicators were not associated with visfatin levels. Regulation of visfatin secretion occurs through biochemical pathways independent from those influenced by pioglitazone or simvastatin.
“…Our findings corroborate with the other study performed with non-diabetic metabolic syndrome patients [24], which demonstrated no difference on visfatin levels after 3 months of treatment. In contrast, Kadoglou et al found a significant reduction (29.7%) of visfatin levels in T2DM patients treated with atorvastatin for 12 weeks [23] and Kostapanos et al observed the same in hyperlipidemic patients treated for 12 weeks with rosuvastatin [25].…”
Section: Discussionsupporting
confidence: 93%
“…To our knowledge, this is the first study to evaluate the simvastatin effect in women without hypertension, dyslipidemia and diabetes. Since similar research has been performed in subjects with these disorders with contradictory results [23][24][25], our study aims to elucidate if simvastatin treatment modulates visfatin levels in women presenting only obesity.…”
These findings suggest that visfatin is not modulated by simvastatin treatment in this group but the treatment may interfere on the relation among visfatin, BMI, insulin and HOMA-IR.
“…Our findings corroborate with the other study performed with non-diabetic metabolic syndrome patients [24], which demonstrated no difference on visfatin levels after 3 months of treatment. In contrast, Kadoglou et al found a significant reduction (29.7%) of visfatin levels in T2DM patients treated with atorvastatin for 12 weeks [23] and Kostapanos et al observed the same in hyperlipidemic patients treated for 12 weeks with rosuvastatin [25].…”
Section: Discussionsupporting
confidence: 93%
“…To our knowledge, this is the first study to evaluate the simvastatin effect in women without hypertension, dyslipidemia and diabetes. Since similar research has been performed in subjects with these disorders with contradictory results [23][24][25], our study aims to elucidate if simvastatin treatment modulates visfatin levels in women presenting only obesity.…”
These findings suggest that visfatin is not modulated by simvastatin treatment in this group but the treatment may interfere on the relation among visfatin, BMI, insulin and HOMA-IR.
“…Our study design cannot explain causality. Further interventional studies to decrease visfatin levels [19,20] are needed to explore histopathological improvements in liver biopsy. Moreover, visfatin levels could predict the presence of the portal inflammation, this molecule could involve a non-invasive technical to determine this pathological change.…”
The mean age was 42.8 +/- 11.2 years, the mean BMI was 33.1 +/- 10.2 with 37 males (67.3%) and 18 females (32.7%). Probabilities to have; portal inflammation increased 1.11 (CI95%:1.03-1.50) with each increment of 1 ng/ml of visfatin concentration, high grade of steatosis increased 1.25 (CI 95%:1.06-1.61) with each unit of insulin concentrations, fibrosis increased 1.12 (CI 95%:1.02-1.43) with each unit of fat mass and lobulillar inflammation increased 13.4 (CI 95%:1.3-147) with each unit of HOMA-IR. Portal inflammation frequencies were different between groups (low visfatin group 13.07 < ng/ml: 37.5% versus high visfatin group 13.07 > ng/ml: 62.5%; P < 0.05). In conclusion, several histopathological changes in liver biopsies could be explained by insulin concentrations, HOMA-IR, and fat mass amount. Moreover, visfatin plasma concentrations could predict the presence of portal inflammation in NAFLD patients.
“…2). Pooled results with only double-blinded, placebo-controlled trials [13–16, 18, 23] retrieved similar results (WMD: -0.15 μg/mL; 95% CI, -0.64–0.34 μg/mL; p = 0.54).Fig. 2Forest plot for the estimation of the effect of simvastatin treatment of serum adiponectin stratified by the treatment duration
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BackgroundEffects of simvastatin on serum level of adiponectin, a protein conferring benefits in both cardiovascular and metabolic system, are not fully determined.MethodsA meta-analysis of randomized controlled trials (RCTs) was performed. Studies were identified by searching of Pubmed, Embase, and the Cochrane Library databases. Heterogeneity among the RCTs was determined by Cochrane’s Q test and I2 statistics. Meta-analysis was performed with random-effect model or fixed-effect model according to the heterogeneity. Meta-regression and subgroup analyses were performed to analyze the source of heterogeneity.ResultsTwelve RCTs with 16 comparisons and 1042 patients were included. Overall, serum adiponectin was not significantly affected by simvastatin (WMD: 0.42 μg/mL; 95% CI, -0.66–1.50 μg/mL). However, significant heterogeneity was detected (Cochrane’s Q test: p < 0.01; I2 = 83%). Subsequent meta-regression analyses indicated that treatment duration was a significant determinant of the effects of simvastatin treatment on serum adiponectin (Coefficient 0.04, p = 0.03). Subgroup analyses demonstrated that simvastatin treatment was associated with increased adiponectin in studies with treatment duration of 12 weeks (WMD: 3.65 μg/mL; p < 0.01), but not in studies with treatment duration of ≤ 8 weeks (WMD: -0.20 μg/mL; p = 0.38). The different between the two stratums was significant (p < 0.01).ConclusionsTreatment with simvastatin of 12 weeks may increase the serum level adiponectin in patients at risk for cardiovascular diseases, but not for the short term treatment of ≤ 8 weeks.
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