Osteoclastic function is accelerated in male patients with type 2 diabetes mellitus: the preventive role of osteoclastogenesis inhibitory factor/osteoprotegerin (OCIF/OPG) on the decrease of bone mineral density.
To clarify the pathogenesis of altered bone metabolism in diabetic state and its underlying mechanisms, the bone mineral content and fasting levels of serum intact parathyroid hormone (i-PTH), intact osteocalcin (i-OC), tartrate-resistant acid phosphatase (TRAP) and osteoclastgenesis inhibitory factor/osteoprotegerin (OCIF/OPG) were measured in male type 2 diabetic patients and their age-matched controls. In addition, urine levels of osteoclastic markers, C-telopeptide of type I collagen (CTx), deoxypyridinoline (DPD), and N-telopeptide of type I collagen (NTx) were simultaneously determined. Serum levels of i-PTH and i-OC in diabetic patients were significantly lower than those in the controls. Conversely, serum concentrations of TRAP were significantly elevated in diabetic patients. However, no clear correlation was observed between serum i-OC and TRAP. It was also observed that urinary excretion of CTx, DPD, and NTx was significantly increased in the diabetics as compared with the controls. Unexpectedly, serum levels of OCIF/OPG tended to be higher in the diabetic group, and these values exhibited a significantly positive correlation with those of serum TRAP. There was found a significantly negative correlation between serum TRAP and bone mineral density (BMD) and also between serum OCIF/OPG and bone mineral density. It seems probable that OCIF/OPG has a suppressive role on the increased bone resorption to prevent further loss of the skeletal bone mass in type 2 diabetic patients.
Suzuki
Kiyoshi
K
Third Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan.
Kurose
Takeshi
T
Takizawa
Makoto
M
Maruyama
Masahiro
M
Ushikawa
Kenji
K
Kikuyama
Munetsugu
M
Sugimoto
Chieko
C
Seino
Yutaka
Y
Nagamatsu
Shinya
S
Ishida
Hitoshi
H
D000135:Acid Phosphatase / Q000097:blood; D000596:Amino Acids / Q000652:urine; D015415:Biomarkers / Q000097:blood; D015519:Bone Density / Q000187:drug effects*; D002096:C-Peptide / Q000737:chemistry / Q000652:urine; D002117:Calcitriol / Q000097:blood; D002118:Calcium / Q000097:blood; D003094:Collagen / Q000652:urine; D024042:Collagen Type I; D003627:Data Interpretation, Statistical; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology* / Q000652:urine; D006023:Glycoproteins / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology* / Q000502:physiology; D006801:Humans; D007328:Insulin / Q000097:blood; D007527:Isoenzymes / Q000097:blood; D008274:Magnesium / Q000097:blood; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010010:Osteoclasts / Q000502:physiology*; D053244:Osteoprotegerin; D010281:Parathyroid Hormone / Q000097:blood; D010455:Peptides / Q000652:urine; D010758:Phosphorus / Q000097:blood; D018160:Receptors, Cytoplasmic and Nuclear / Q000737:chemistry / Q000378:metabolism / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000737:chemistry / Q000378:metabolism / Q000502:physiology; D012737:Sex Factors; D000071681:Tartrate-Resistant Acid Phosphatase
D000596:Amino Acids; D015415:Biomarkers; D002096:C-Peptide; D024042:Collagen Type I; D006023:Glycoproteins; D007328:Insulin; D007527:Isoenzymes; D053244:Osteoprotegerin; D010281:Parathyroid Hormone; D010455:Peptides; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human; C052929:collagen type I trimeric cross-linked peptide; D015675:Osteocalcin; D010758:Phosphorus; C036020:deoxypyridinoline; D003094:Collagen; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D002117:Calcitriol; D008274:Magnesium; D002118:Calcium