title: Correlation between adiponectin and reduction of cell adhesion molecules after pitavastatin treatment in hyperlipidemic patients with type 2 diabetes mellitus.
abstract: The aim of this study was to determine whether pitavastatin may prevent the progression of atherosclerotic changes in hyperlipidemic patients. Seventy-five hyperlipidemic patients with and without type 2 diabetes were enrolled to receive pitavastatin 2 mg daily. Cell adhesion molecules (sCD40L, sP-selectin, sE-selectin, and sL-selectin), chemokines (MCP-1 and RANTES) and adiponectin were measured at baseline and after 3 and 6 months of pitavastatin treatment. Adiponectin levels prior to pitavastatin treatment in hyperlipidemic patients with and without diabetes were lower than levels in normolipidemic controls. Both total cholesterol and the LDL-cholesterol (LDL-C) decreased significantly after pitavastatin administration. Additionally, hyperlipidemic patients with type 2 diabetes exhibited a significant increase in adiponectin levels after pitavastatin treatment (before vs. 3 months, 6 months, 2.81+/-0.95 vs. 3.84+/-0.84 microg/ml (p<0.01), 4.61+/-1.15 mug/ml (p<0.001)). Furthermore, hyperlipidemic diabetics exhibited significant decreases in sE-selectin and sL-selectin levels after 6 months of pitavastatin treatment (sE-selectin, before vs. 6 months, 74+/-21 vs. 51+/-10 ng/ml, p<0.05; sL-selectin, before vs. 6 months, 896+/-141 vs. 814+/-129 ng/ml, p<0.05). In addition, adiponectin showed significant correlation with sE-selectin and sL-selectin in diabetic hyperlipidemia. However, MCP-1, RANTES and sCD40L did not exhibit any differences before or after pitavastatin administration. These results suggest that pitavastatin possesses an adiponectin-dependent anti-atherosclerotic effect in hyperlipidemic patients with type 2 diabetes in addition to its lowering effects on total cholesterol and LDL-C.
authors.affiliation: Division of Hematology, Kishiwada City Hospital, 1001 Gakuhara-cho, Kishiwada, Osaka 596-8501, Japan. shosaku-n@mbp.ocn.ne.jp
authors.forename: Shosaku
authors.initials: S
authors.lastname: Nomura
authors.forename: Akira
authors.initials: A
authors.lastname: Shouzu
authors.forename: Seitarou
authors.initials: S
authors.lastname: Omoto
authors.forename: Norihito
authors.initials: N
authors.lastname: Inami
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tanaka
authors.forename: Masashi
authors.initials: M
authors.lastname: Nanba
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Shouda
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Takahashi
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kimura
authors.forename: Toshiji
authors.initials: T
authors.lastname: Iwasaka
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D000368:Aged; D023201:CD40 Ligand / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood*; D018946:Chemokine CCL5 / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications*; D019040:E-Selectin / Q000097:blood; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D011804:Quinolines / Q000627:therapeutic use*; D054390:Receptors, CCR2 / Q000097:blood; D012016:Reference Values; D012907:Smoking / Q000453:epidemiology
chemical_list: D052242:Adiponectin; D023201:CD40 Ligand; D015815:Cell Adhesion Molecules; D018946:Chemokine CCL5; D008078:Cholesterol, LDL; D019040:E-Selectin; D006442:Glycated Hemoglobin; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019007:P-Selectin; D011804:Quinolines; D054390:Receptors, CCR2; C108475:pitavastatin