title: Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism.
abstract: OBJECTIVE
  Postprandial suppression of bone resorption is considered one of the main contributors in the circadian rhythm of bone turnover markers. The aim of this study was to investigate this physiological response of bone tissue in diseases that affect bone metabolism.
  
  
  METHODS
  In this study, 118 patients (45 hypothyroid, 40 hyperthyroid, and 33 β-thalassemic patients) and 78 healthy individuals matched for age and body mass index were included. An oral glucose test (75 g glucose) was performed after overnight fasting. Serum levels of procollagen type-I N-terminal propeptide (P1NP), β-C-terminal telopeptide of type I collagen (β-CTX), and osteocalcin were assayed at 0, 60, and 120 min.
  
  
  RESULTS
  Baseline values of bone turnover markers were significantly elevated in hyperthyroid and β-thalassemic patients but not in hypothyroid patients compared with the control group. After oral glucose, the levels of β-CTX but not P1NP or osteocalcin were significantly suppressed in all groups (mean change from baseline is 46.9% for β-CTX, 7.9% for P1NP, and 8% for osteocalcin). The percentage change from baseline for β-CTX was significantly augmented in hypothyroidism (52 vs 42%, P=0.009).
  
  
  CONCLUSIONS
  The preservation or even augmentation of postprandial suppression of bone resorption in diseases that affect bone metabolism through distinct pathogenetic mechanisms suggests the importance of this physiological response to nutrients for the general homeostasis and functional integrity of the skeleton.
authors.affiliation: Division of Endocrinology and Metabolism, AHEPA University Hospital, Aristotle University of Thessaloniki, 1. S. Kyriakidi Street, 54636 Thessaloniki, Greece. margia@med.auth.gr
authors.forename: Maria P
authors.initials: MP
authors.lastname: Yavropoulou
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Tomos
authors.forename: Xanthippi
authors.initials: X
authors.lastname: Tsekmekidou
authors.forename: Olympia
authors.initials: O
authors.lastname: Anastasiou
authors.forename: Pantelis
authors.initials: P
authors.lastname: Zebekakis
authors.forename: Michael
authors.initials: M
authors.lastname: Karamouzis
authors.forename: Anna
authors.initials: A
authors.lastname: Gotzamani-Psarrakou
authors.forename: Eleni
authors.initials: E
authors.lastname: Chassapopoulou
authors.forename: Panagiota
authors.initials: P
authors.lastname: Chalkia
authors.forename: John G
authors.initials: JG
authors.lastname: Yovos
mesh_terms: D015415:Biomarkers / Q000032:analysis; D001846:Bone Development / Q000502:physiology*; D001851:Bone Diseases, Metabolic / Q000175:diagnosis / Q000378:metabolism*; D001842:Bone and Bones / Q000378:metabolism*; D024042:Collagen Type I / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D005951:Glucose Tolerance Test; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood; D007037:Hypothyroidism / Q000097:blood; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D011347:Procollagen / Q000097:blood; D017086:beta-Thalassemia / Q000378:metabolism
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D011347:Procollagen; D015675:Osteocalcin; D005947:Glucose