[Poor bone quality in diabetes and arterioscelerosis].
Type 1 and 2 diabetes deteriorate bone quality in terms of collagen cross-links formation in bone, Recently, we demonstrate that hyperhomocysteinemia also resulted in collagen cross-link abnormalities in bone (Saito M, Osteoporos Int, 2009 in press) . Hyperglycemia, oxidative stress, and hyperhomocysteinemia induce the reduction in enzymatic cross-links and the accumulation of non-enzymatic cross-link, Advanced glycation end products (AGEs, Pentosidine) in bone. In this review, I describe that diabetes and hyperhomocysteinemia are crucial determinants of detrimental crosslinking of bone collagen that have been reported in the literature.
Saito
Mitsuru
M
Department of Orthopaedic Surgery, Jikei University School of Medicine.
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000652:urine; D001161:Arteriosclerosis / Q000150:complications / Q000378:metabolism*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D015519:Bone Density; D003094:Collagen / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism*; D050723:Fractures, Bone / Q000209:etiology; D017127:Glycation End Products, Advanced / Q000652:urine; D006710:Homocysteine / Q000097:blood; D006801:Humans; D008239:Lysine / Q000031:analogs & derivatives / Q000652:urine; D010024:Osteoporosis / Q000175:diagnosis / Q000209:etiology*; D012306:Risk
D015415:Biomarkers; D017127:Glycation End Products, Advanced; D006710:Homocysteine; D003094:Collagen; D001120:Arginine; C062187:pentosidine; D008239:Lysine