title: Effects of pioglitazone on serum fetuin-A levels in patients with type 2 diabetes mellitus.
abstract: Fetuin-A (alpha2-Heremans-Schmid glycoprotein), a circulating glycoprotein, can inhibit insulin signaling both in vivo and in vitro. Recently, we and another independent group have shown that fetuin-A is positively associated with insulin resistance in humans. Furthermore, it has been reported that higher fetuin-A levels are associated with metabolic syndrome and atherogenic lipid profiles. These data suggest that fetuin-A might be a regulator of insulin resistance and/or metabolic syndrome. However, it is not clear how fetuin-A levels are regulated. To address this, we investigated the effects of representative insulin-sensitizing therapies such as pioglitazone, metformin, and aerobic exercise on fetuin-A levels. Twenty-seven patients with type 2 diabetes mellitus were divided into pioglitazone-treated (Pio), metformin-treated (Met), and exercise-treated (Ex) groups. Ten patients in the Pio group and 9 patients in the Met group took 15 or 30 mg/d pioglitazone or 500 or 750 mg/d metformin, respectively, for 6 months. Eight patients in the Ex group underwent a 3-month aerobic exercise program. Serum fetuin-A levels were measured before and after each intervention. Intervention significantly decreased hemoglobin A(1c) in all groups. After treatment, serum fetuin-A levels significantly decreased in the Pio group (291.2 +/- 57.7 to 253.1 +/- 43.9 microg/mL, P = .006), whereas there were no changes in serum fetuin-A after intervention in either the Met or the Ex groups. We hypothesize that pioglitazone could partially ameliorate insulin resistance via modulating fetuin-A levels.
authors.affiliation: Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan. ktmori@med.osaka-cu.ac.jp
authors.forename: Katsuhito
authors.initials: K
authors.lastname: Mori
authors.forename: Masanori
authors.initials: M
authors.lastname: Emoto
authors.forename: Takahiro
authors.initials: T
authors.lastname: Araki
authors.forename: Hisayo
authors.initials: H
authors.lastname: Yokoyama
authors.forename: Eiko
authors.initials: E
authors.lastname: Lee
authors.forename: Megumi
authors.initials: M
authors.lastname: Teramura
authors.forename: Hidenori
authors.initials: H
authors.lastname: Koyama
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Shoji
authors.forename: Masaaki
authors.initials: M
authors.lastname: Inaba
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Nishizawa
mesh_terms: D000368:Aged; D001798:Blood Proteins / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D015444:Exercise; D005081:Exercise Therapy; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007333:Insulin Resistance; D008297:Male; D008687:Metformin / Q000627:therapeutic use; D008875:Middle Aged; D000077205:Pioglitazone; D045162:Thiazolidinediones / Q000627:therapeutic use; D060749:alpha-2-HS-Glycoprotein
chemical_list: C556354:AHSG protein, human; D001798:Blood Proteins; D007004:Hypoglycemic Agents; D045162:Thiazolidinediones; D060749:alpha-2-HS-Glycoprotein; D008687:Metformin; D000077205:Pioglitazone