Comparison of the effect of lipophilic and hydrophilic statins on serum adiponectin levels in patients with mild hypertension and dyslipidemia: Kinki Adiponectin Interventional (KAI) Study.
The plasma level of adiponectin, which is known as an anti-atherogenic adipocytokine, correlates inversely with the progression of atherosclerosis. An increase in the serum adiponectin level has been reported after the administration of hydrophilic pravastatin, but not after the administration of lipophilic statins thus far. We investigated whether hydrophilic pravastatin acts distinctly from simvastatin, which has the highest lipophilicity, on the favorable effect on adiponectin in dyslipidemic patients. A total of 27 dyslipidemic patients with mild hypertension were enrolled in this study. The patients were initially treated with simvastatin 10 mg/day for six months or more (mean 7.1 months), and then were switched to pravastatin 20 mg/day. The serum adiponectin, cholesterol fractionated components, and C-reactive protein (CRP) were evaluated after six-month intervals. Switching from simvastatin to pravastatin caused little change in the low-density lipoprotein cholesterol levels (103 mg/dl to 104 mg/dl, p = 0.782) and blood pressure (133/70 mmHg to 132/69 mmHg), while the serum adiponectin level significantly increased (11.9 mug/ml to 13.1 mug/ml, p = 0.009, respectively), and the serum CRP significantly decreased (0.078 mg/dl to 0.062 mg/dl, p = 0.040, respectively). Hydrophilic pravastatin increased the serum adiponectin level and decreased the CRP after switching from lipophilic simvastatin in the absence of any difference in the low-density lipoprotein cholesterol level and blood pressure. It remains possible, however, that this difference was due not only to pharmacologic lipophilicity, but also to some other specific characteristics such as the formula of statins, the subject characteristics, race, body size, high-density lipoprotein cholesterol, etc.
Department of Vascular and Geriatric Medicine, Kinki University School of Medicine, Osaka-sayama, Osaka, Japan. tkai@med.kindai.ac.jp
Tatsuya
T
Kai
Shuji
S
Arima
Yoshihiro
Y
Taniyama
Mari
M
Nakabou
Ken
K
Kanamasa
D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D050171:Dyslipidemias / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D005260:Female; D006801:Humans; D057927:Hydrophobic and Hydrophilic Interactions; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000737:chemistry / Q000493:pharmacokinetics / Q000494:pharmacology*; D006973:Hypertension / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000737:chemistry / Q000493:pharmacokinetics / Q000494:pharmacology; D011446:Prospective Studies; D019821:Simvastatin / Q000737:chemistry / Q000493:pharmacokinetics / Q000494:pharmacology
C499918:ADIPOQ protein, human; D052242:Adiponectin; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein; D002784:Cholesterol; D019821:Simvastatin; D017035:Pravastatin