title: Increased bone resorption may play a crucial role in the occurrence of osteopenia in patients with type 2 diabetes: Possible involvement of accelerated polyol pathway in its pathogenesis.
abstract: In order to investigate the underlying mechanism of alterations in bone mineral metabolism in patients with type 2 diabetes, we determined circulating levels of bone functional markers along with urinary excretion of sorbitol (SOR) and bone mineral density (BMD), and also examined their mutual interrelationship. A total of 151 male type 2 diabetic patients were examined in this study. Forty-eight age-matched male healthy subjects were also studied as the controls. A significant reduction of serum intact osteocalcin (i-OC) was found in the diabetic groups (p<0.01). On the other hand, circulating levels of tartrate resistant acid phosphatase (TRAP) in the diabetic patients were significantly higher than those in the controls (p<0.01). Interestingly, a significantly negative relationship was observed between BMD and serum TRAP (p<0.01), although no significant relationship was noted between BMD and serum i-OC in diabetic patients. Urinary excretion of SOR was significantly elevated in the diabetic patients when compared with the controls (p<0.01). In addition, a significantly positive correlation was observed between serum TRAP and urinary SOR (p<0.01), but not between serum i-OC and urinary SOR. Elevated serum TRAP in diabetes was reduced after the administration of aldose reductase inhibitor (p<0.05). It seems most likely that the increase in osteoclastic function probably due to accelerated polyol pathway plays a crucial role in the pathogenesis of decreased bone mineral content in male patients with type 2 diabetes.
authors.affiliation: Third Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Takizawa
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Suzuki
authors.forename: Tadashi
authors.initials: T
authors.lastname: Matsubayashi
authors.forename: Munetsugu
authors.initials: M
authors.lastname: Kikuyama
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Suzuki
authors.forename: Kazuto
authors.initials: K
authors.lastname: Takahashi
authors.forename: Hidenori
authors.initials: H
authors.lastname: Katsuta
authors.forename: Junko
authors.initials: J
authors.lastname: Mitsuhashi
authors.forename: Susumu
authors.initials: S
authors.lastname: Nishida
authors.forename: Shinya
authors.initials: S
authors.lastname: Yamaguchi
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Yoshimoto
authors.forename: Eiji
authors.initials: E
authors.lastname: Itagaki
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ishida
mesh_terms: D000135:Acid Phosphatase / Q000097:blood; D015519:Bone Density; D001851:Bone Diseases, Metabolic / Q000097:blood* / Q000209:etiology / Q000378:metabolism; D001862:Bone Resorption / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications / Q000378:metabolism; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D007064:L-Iditol 2-Dehydrogenase / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood*; D011108:Polymers / Q000378:metabolism; D015398:Signal Transduction; D013012:Sorbitol / Q000097:blood / Q000378:metabolism / Q000652:urine; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D007527:Isoenzymes; D011108:Polymers; C024617:polyol; D015675:Osteocalcin; D013012:Sorbitol; D007064:L-Iditol 2-Dehydrogenase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase