title: Anti-inflammatory effects of simvastatin on adipokines in type 2 diabetic patients with carotid atherosclerosis.
abstract: OBJECTIVE
  Statins are extensively used for lowering LDL-cholesterol and reducing cardiovascular events. Recent studies have shown that statins have beneficial anti-inflammatory effects. We aimed to determine whether and how adipokines are regulated during statin treatment in type 2 diabetic patients.
  
  
  METHODS
  In this study,we investigated the changes of CRP and inflammation-related adipokines (SAA,IL-6,TNFalpha and adiponectin) in 23 type 2 diabetic patients with atherosclerosis who received statin therapy, and 20 diabetic patients with atherosclerosis and 14 diabetic patients without atherosclerosis who did not receive statin therapy for a period of three months.
  
  
  RESULTS
  By the end of the simvastatin treatment (40 mg, daily), LDL-cholesterol was decreased by 16.7% and HDL-cholesterol was increased by 31.9%. SAA, CRP, TNFalpha and IL-6 levels were decreased by 31.8%, 66.2%, 53.9% and 14%, respectively and adiponectin was increased by 59.6%, compared with the baseline levels. Interestingly, the decrease of SAA was positively correlated with that of LDL-cholesterol but negatively with HDL-cholesterol during statin treatment. Among the adipokines, the decrease of SAA was positively correlated with TNFalpha (r = 0.50, p = 0.016).
  
  
  CONCLUSIONS
  The results suggest that adipokines may be differentially regulated and independent of cholesterol changes and that adipokines may be a mediator, and the adipose tissue may be a target of statins' anti-inflammatory effect.
authors.affiliation: Division of Endocrinology, The Affliated Drum Tower Hospital of Nanjing University, Nanjing 210008, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Hu
authors.forename: Guoyu
authors.initials: G
authors.lastname: Tong
authors.forename: Wei
authors.initials: W
authors.lastname: Xu
authors.forename: Jiajia
authors.initials: J
authors.lastname: Pan
authors.forename: Kathy
authors.initials: K
authors.lastname: Ryan
authors.forename: Rongze
authors.initials: R
authors.lastname: Yang
authors.forename: Alan R
authors.initials: AR
authors.lastname: Shuldiner
authors.forename: Da-Wei
authors.initials: DW
authors.lastname: Gong
authors.forename: Dalong
authors.initials: D
authors.lastname: Zhu
mesh_terms: D054392:Adipokines / Q000097:blood*; D052242:Adiponectin / Q000097:blood; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000378:metabolism; D019821:Simvastatin / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: C499918:ADIPOQ protein, human; D054392:Adipokines; D052242:Adiponectin; D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D019821:Simvastatin