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[Poor bone quality in diabetes and arterioscelerosis].

Abstract
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.
AuthorsMitsuru Saito
JournalClinical calcium (Clin Calcium) Vol. 19 Issue 9 Pg. 1257-68 (Sep 2009) ISSN: 0917-5857 [Print] Japan
PMID19721196 (Publication Type: Journal Article, Review)
Chemical References
  • Biomarkers
  • Glycation End Products, Advanced
  • Homocysteine
  • Collagen
  • Arginine
  • pentosidine
  • Lysine
Topics
  • Animals
  • Arginine (analogs & derivatives, urine)
  • Arteriosclerosis (complications, metabolism)
  • Biomarkers (blood, urine)
  • Bone Density
  • Collagen (metabolism)
  • Diabetes Complications
  • Diabetes Mellitus (metabolism)
  • Fractures, Bone (etiology)
  • Glycation End Products, Advanced (urine)
  • Homocysteine (blood)
  • Humans
  • Lysine (analogs & derivatives, urine)
  • Osteoporosis (diagnosis, etiology)
  • Risk

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