Piotr Chruściel1, Amirhossein Sahebkar2, Magdalena Rembek-Wieliczko3, Maria-Corina Serban4, Sorin Ursoniu5, Dimitri P Mikhailidis6, Steven R Jones7, Svetlana Mosteoru8, Michael J Blaha7, Seth S Martin7, Jacek Rysz3, Peter P Toth9, Gregory Y H Lip10, Michael J Pencina11, Kausik K Ray12, Maciej Banach13. 1. Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland. 2. Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Metabolic Research Centre, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia. 3. Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland; Healthy Aging Research Centre (HARC), Lodz, Poland. 4. Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Functional Sciences, Discipline of Pathophysiology, "Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania. 5. Department of Functional Sciences, Discipline of Public Health, "Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania. 6. Department of Clinical Biochemistry, Royal Free Campus, University College London Medical School, University College London (UCL), London, UK. 7. The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. 8. Institute for Cardiovascular Medicine Timisoara, Cardiology Department, University of Medicine and Pharmacy "Victor Babes", Timisoara, Romania. 9. The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA; Preventive Cardiology, CGH Medical Center, Sterling, IL, USA. 10. University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK. 11. Duke Clinical Research Institute, Department of Biostatistics and Bioinformatics, Duke University, Durham, NC, USA. 12. Department of Primary Care and Public Health, School of Public Health, Imperial College London, UK. 13. Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland; Healthy Aging Research Centre (HARC), Lodz, Poland. Electronic address: maciejbanach@aol.co.uk.
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.
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.
Authors: John S Kim; Michaela R Anderson; Anna J Podolanczuk; Steven M Kawut; Matthew A Allison; Ganesh Raghu; Karen Hinckley-Stuckovsky; Eric A Hoffman; Russell P Tracy; R Graham Barr; David J Lederer; Jon T Giles Journal: Chest Date: 2019-10-31 Impact factor: 9.410