Impact of statin therapy on plasma adiponectin concentrations: A systematic review and meta-analysis of 43 randomized controlled trial arms

The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs). Quantitative data synthesis was performed using a random-effects mo...

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Published in:Atherosclerosis Vol. 253; pp. 194 - 208
Main Authors: Chruściel, Piotr, Sahebkar, Amirhossein, Rembek-Wieliczko, Magdalena, Serban, Maria-Corina, Ursoniu, Sorin, Mikhailidis, Dimitri P., Jones, Steven R., Mosteoru, Svetlana, Blaha, Michael J., Martin, Seth S., Rysz, Jacek, Toth, Peter P., Lip, Gregory Y.H., Pencina, Michael J., Ray, Kausik K., Banach, Maciej
Format: Journal Article
Language:English
Published: Ireland Elsevier B.V 01.10.2016
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ISSN:0021-9150, 1879-1484, 1879-1484
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Abstract The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs). Quantitative data synthesis was performed using a random-effects model with weighted mean difference (WMD) and 95% confidence interval (CI) as summary statistics. In 30 studies (43 study arms) with 2953 participants, a significant increase in plasma adiponectin levels was observed after statin therapy (WMD: 0.57 μg/mL, 95% CI: 0.18, 0.95, p = 0.004). In subgroup analysis, atorvastatin, simvastatin, rosuvastatin, pravastatin and pitavastatin were found to change plasma adiponectin concentrations by 0.70 μg/mL (95% CI: −0.26, 1.65), 0.50 μg/mL (95% CI: −0.44, 1.45), −0.70 μg/mL (95% CI: −1.08, −0.33), 0.62 μg/mL (95% CI: −0.12, 1.35), and 0.51 μg/mL (95% CI: 0.30, 0.72), respectively. With respect to duration of treatment, there was a significant increase in the subset of trials lasting ≥12 weeks (WMD: 0.88 μg/mL, 95% CI: 0.19, 1.57, p = 0.012) but not in the subset of <12 weeks of duration (WMD: 0.18 μg/mL, 95% CI: −0.23, 0.58, p = 0.390). Random-effects meta-regression suggested a significant association between statin-induced elevation of plasma adiponectin and changes in plasma low density lipoprotein cholesterol levels (slope: 0.04; 95% CI: 0.01, 0.06; p = 0.002). The meta-analysis showed a significant increase in plasma adiponectin levels following statin therapy. Although statins are known to increase the risk for new onset diabetes mellitus, our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression. [Display omitted] •The effect of statin therapy on plasma adiponectin levels has not been conclusively studied.•The analysis shows a significant increase in plasma adiponectin levels after statin therapy (WMD: +0.57 μg/mL).•The meta-analysis confirmed that statins may have an important impact on the adiponectin levels.•The pleiotropic adiponectin-elevating effect of statins might explain the benefits of statins in reducing the CV risk.
AbstractList The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs). Quantitative data synthesis was performed using a random-effects model with weighted mean difference (WMD) and 95% confidence interval (CI) as summary statistics. In 30 studies (43 study arms) with 2953 participants, a significant increase in plasma adiponectin levels was observed after statin therapy (WMD: 0.57 μg/mL, 95% CI: 0.18, 0.95, p = 0.004). In subgroup analysis, atorvastatin, simvastatin, rosuvastatin, pravastatin and pitavastatin were found to change plasma adiponectin concentrations by 0.70 μg/mL (95% CI: −0.26, 1.65), 0.50 μg/mL (95% CI: −0.44, 1.45), −0.70 μg/mL (95% CI: −1.08, −0.33), 0.62 μg/mL (95% CI: −0.12, 1.35), and 0.51 μg/mL (95% CI: 0.30, 0.72), respectively. With respect to duration of treatment, there was a significant increase in the subset of trials lasting ≥12 weeks (WMD: 0.88 μg/mL, 95% CI: 0.19, 1.57, p = 0.012) but not in the subset of <12 weeks of duration (WMD: 0.18 μg/mL, 95% CI: −0.23, 0.58, p = 0.390). Random-effects meta-regression suggested a significant association between statin-induced elevation of plasma adiponectin and changes in plasma low density lipoprotein cholesterol levels (slope: 0.04; 95% CI: 0.01, 0.06; p = 0.002). The meta-analysis showed a significant increase in plasma adiponectin levels following statin therapy. Although statins are known to increase the risk for new onset diabetes mellitus, our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression. [Display omitted] •The effect of statin therapy on plasma adiponectin levels has not been conclusively studied.•The analysis shows a significant increase in plasma adiponectin levels after statin therapy (WMD: +0.57 μg/mL).•The meta-analysis confirmed that statins may have an important impact on the adiponectin levels.•The pleiotropic adiponectin-elevating effect of statins might explain the benefits of statins in reducing the CV risk.
The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs). Quantitative data synthesis was performed using a random-effects model with weighted mean difference (WMD) and 95% confidence interval (CI) as summary statistics. In 30 studies (43 study arms) with 2953 participants, a significant increase in plasma adiponectin levels was observed after statin therapy (WMD: 0.57 μg/mL, 95% CI: 0.18, 0.95, p = 0.004). In subgroup analysis, atorvastatin, simvastatin, rosuvastatin, pravastatin and pitavastatin were found to change plasma adiponectin concentrations by 0.70 μg/mL (95% CI: -0.26, 1.65), 0.50 μg/mL (95% CI: -0.44, 1.45), -0.70 μg/mL (95% CI: -1.08, -0.33), 0.62 μg/mL (95% CI: -0.12, 1.35), and 0.51 μg/mL (95% CI: 0.30, 0.72), respectively. With respect to duration of treatment, there was a significant increase in the subset of trials lasting ≥12 weeks (WMD: 0.88 μg/mL, 95% CI: 0.19, 1.57, p = 0.012) but not in the subset of <12 weeks of duration (WMD: 0.18 μg/mL, 95% CI: -0.23, 0.58, p = 0.390). Random-effects meta-regression suggested a significant association between statin-induced elevation of plasma adiponectin and changes in plasma low density lipoprotein cholesterol levels (slope: 0.04; 95% CI: 0.01, 0.06; p = 0.002). The meta-analysis showed a significant increase in plasma adiponectin levels following statin therapy. Although statins are known to increase the risk for new onset diabetes mellitus, our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression.
Abstract Background and aims The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs). Methods Quantitative data synthesis was performed using a random-effects model with weighted mean difference (WMD) and 95% confidence interval (CI) as summary statistics. Results In 30 studies (43 study arms) with 2953 participants, a significant increase in plasma adiponectin levels was observed after statin therapy (WMD: 0.57 μg/mL, 95% CI: 0.18, 0.95, p  = 0.004). In subgroup analysis, atorvastatin, simvastatin, rosuvastatin, pravastatin and pitavastatin were found to change plasma adiponectin concentrations by 0.70 μg/mL (95% CI: −0.26, 1.65), 0.50 μg/mL (95% CI: −0.44, 1.45), −0.70 μg/mL (95% CI: −1.08, −0.33), 0.62 μg/mL (95% CI: −0.12, 1.35), and 0.51 μg/mL (95% CI: 0.30, 0.72), respectively. With respect to duration of treatment, there was a significant increase in the subset of trials lasting ≥12 weeks (WMD: 0.88 μg/mL, 95% CI: 0.19, 1.57, p  = 0.012) but not in the subset of <12 weeks of duration (WMD: 0.18 μg/mL, 95% CI: −0.23, 0.58, p  = 0.390). Random-effects meta-regression suggested a significant association between statin-induced elevation of plasma adiponectin and changes in plasma low density lipoprotein cholesterol levels (slope: 0.04; 95% CI: 0.01, 0.06; p  = 0.002). Conclusions The meta-analysis showed a significant increase in plasma adiponectin levels following statin therapy. Although statins are known to increase the risk for new onset diabetes mellitus, our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression.
The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs).BACKGROUND AND AIMSThe effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs).Quantitative data synthesis was performed using a random-effects model with weighted mean difference (WMD) and 95% confidence interval (CI) as summary statistics.METHODSQuantitative data synthesis was performed using a random-effects model with weighted mean difference (WMD) and 95% confidence interval (CI) as summary statistics.In 30 studies (43 study arms) with 2953 participants, a significant increase in plasma adiponectin levels was observed after statin therapy (WMD: 0.57 μg/mL, 95% CI: 0.18, 0.95, p = 0.004). In subgroup analysis, atorvastatin, simvastatin, rosuvastatin, pravastatin and pitavastatin were found to change plasma adiponectin concentrations by 0.70 μg/mL (95% CI: -0.26, 1.65), 0.50 μg/mL (95% CI: -0.44, 1.45), -0.70 μg/mL (95% CI: -1.08, -0.33), 0.62 μg/mL (95% CI: -0.12, 1.35), and 0.51 μg/mL (95% CI: 0.30, 0.72), respectively. With respect to duration of treatment, there was a significant increase in the subset of trials lasting ≥12 weeks (WMD: 0.88 μg/mL, 95% CI: 0.19, 1.57, p = 0.012) but not in the subset of <12 weeks of duration (WMD: 0.18 μg/mL, 95% CI: -0.23, 0.58, p = 0.390). Random-effects meta-regression suggested a significant association between statin-induced elevation of plasma adiponectin and changes in plasma low density lipoprotein cholesterol levels (slope: 0.04; 95% CI: 0.01, 0.06; p = 0.002).RESULTSIn 30 studies (43 study arms) with 2953 participants, a significant increase in plasma adiponectin levels was observed after statin therapy (WMD: 0.57 μg/mL, 95% CI: 0.18, 0.95, p = 0.004). In subgroup analysis, atorvastatin, simvastatin, rosuvastatin, pravastatin and pitavastatin were found to change plasma adiponectin concentrations by 0.70 μg/mL (95% CI: -0.26, 1.65), 0.50 μg/mL (95% CI: -0.44, 1.45), -0.70 μg/mL (95% CI: -1.08, -0.33), 0.62 μg/mL (95% CI: -0.12, 1.35), and 0.51 μg/mL (95% CI: 0.30, 0.72), respectively. With respect to duration of treatment, there was a significant increase in the subset of trials lasting ≥12 weeks (WMD: 0.88 μg/mL, 95% CI: 0.19, 1.57, p = 0.012) but not in the subset of <12 weeks of duration (WMD: 0.18 μg/mL, 95% CI: -0.23, 0.58, p = 0.390). Random-effects meta-regression suggested a significant association between statin-induced elevation of plasma adiponectin and changes in plasma low density lipoprotein cholesterol levels (slope: 0.04; 95% CI: 0.01, 0.06; p = 0.002).The meta-analysis showed a significant increase in plasma adiponectin levels following statin therapy. Although statins are known to increase the risk for new onset diabetes mellitus, our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression.CONCLUSIONSThe meta-analysis showed a significant increase in plasma adiponectin levels following statin therapy. Although statins are known to increase the risk for new onset diabetes mellitus, our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression.
Author Toth, Peter P.
Rysz, Jacek
Blaha, Michael J.
Banach, Maciej
Sahebkar, Amirhossein
Rembek-Wieliczko, Magdalena
Pencina, Michael J.
Martin, Seth S.
Lip, Gregory Y.H.
Chruściel, Piotr
Ursoniu, Sorin
Jones, Steven R.
Mosteoru, Svetlana
Serban, Maria-Corina
Ray, Kausik K.
Mikhailidis, Dimitri P.
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  surname: Chruściel
  fullname: Chruściel, Piotr
  organization: Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland
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  givenname: Amirhossein
  surname: Sahebkar
  fullname: Sahebkar, Amirhossein
  organization: Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
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  givenname: Magdalena
  surname: Rembek-Wieliczko
  fullname: Rembek-Wieliczko, Magdalena
  organization: Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland
– sequence: 4
  givenname: Maria-Corina
  surname: Serban
  fullname: Serban, Maria-Corina
  organization: Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA
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  givenname: Sorin
  surname: Ursoniu
  fullname: Ursoniu, Sorin
  organization: Department of Functional Sciences, Discipline of Public Health, “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania
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  givenname: Dimitri P.
  surname: Mikhailidis
  fullname: Mikhailidis, Dimitri P.
  organization: Department of Clinical Biochemistry, Royal Free Campus, University College London Medical School, University College London (UCL), London, UK
– sequence: 7
  givenname: Steven R.
  surname: Jones
  fullname: Jones, Steven R.
  organization: The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA
– sequence: 8
  givenname: Svetlana
  surname: Mosteoru
  fullname: Mosteoru, Svetlana
  organization: Institute for Cardiovascular Medicine Timisoara, Cardiology Department, University of Medicine and Pharmacy “Victor Babes”, Timisoara, Romania
– sequence: 9
  givenname: Michael J.
  surname: Blaha
  fullname: Blaha, Michael J.
  organization: The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA
– sequence: 10
  givenname: Seth S.
  surname: Martin
  fullname: Martin, Seth S.
  organization: The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA
– sequence: 11
  givenname: Jacek
  surname: Rysz
  fullname: Rysz, Jacek
  organization: Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland
– sequence: 12
  givenname: Peter P.
  surname: Toth
  fullname: Toth, Peter P.
  organization: The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA
– sequence: 13
  givenname: Gregory Y.H.
  surname: Lip
  fullname: Lip, Gregory Y.H.
  organization: University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK
– sequence: 14
  givenname: Michael J.
  surname: Pencina
  fullname: Pencina, Michael J.
  organization: Duke Clinical Research Institute, Department of Biostatistics and Bioinformatics, Duke University, Durham, NC, USA
– sequence: 15
  givenname: Kausik K.
  surname: Ray
  fullname: Ray, Kausik K.
  organization: Department of Primary Care and Public Health, School of Public Health, Imperial College London, UK
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  givenname: Maciej
  orcidid: 0000-0001-6690-6874
  surname: Banach
  fullname: Banach, Maciej
  email: maciejbanach@aol.co.uk
  organization: Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27498397$$D View this record in MEDLINE/PubMed
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Statins
Adiponectin
Meta-analysis
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Snippet The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic...
Abstract Background and aims The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this...
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SubjectTerms Adiponectin
Adiponectin - blood
Adult
Aged
Atorvastatin - therapeutic use
Cardiovascular
Cardiovascular Diseases - blood
Female
Humans
Hydroxymethylglutaryl-CoA reductase inhibitors
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Male
Meta-analysis
Middle Aged
Pravastatin - therapeutic use
Quinolines - therapeutic use
Randomized Controlled Trials as Topic
Regression Analysis
Rosuvastatin Calcium - therapeutic use
Simvastatin - therapeutic use
Statins
Title Impact of statin therapy on plasma adiponectin concentrations: A systematic review and meta-analysis of 43 randomized controlled trial arms
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https://dx.doi.org/10.1016/j.atherosclerosis.2016.07.897
https://www.ncbi.nlm.nih.gov/pubmed/27498397
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