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. Patients and methods: In this study, 118 patients (45 hypothyroid, 40 hyperthyroid, and 33 b-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), b-C-terminal telopeptide of type I collagen (b-CTX), and osteocalcin were assayed at 0, 60, and 120 min. Results: Baseline values of bone turnover markers were significantly elevated in hyperthyroid and b-thalassemic patients but not in hypothyroid patients compared with the control group. After oral glucose, the levels of b-CTX but not P1NP or osteocalcin were significantly suppressed in all groups (mean change from baseline is 46.9% for b-CTX, 7.9% for P1NP, and 8% for osteocalcin). The percentage change from baseline for b-CTX was significantly augmented in hypothyroidism (52 vs 42%, PZ0.009). Conclusion: 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.

Postprandial response of bone turnover markers in patients with Crohn’s disease

“…The postprandial response of bone turnover is expressed as the percent change from baseline at 2 h after oral glucose for CTX-I and P1NP, as previously described [20,21] . The differences between patients and controls were assessed using a two-tailed Student's t-test or the non-parametric MannWhitney U test for independent samples, as appropriate.…”

“…Two recent studies have investigated the postprandial response of bone resorption in patients with type 2 diabetes mellitus [20] , thyroid diseases and beta-thalassemia major [21] , that are very often complicated with low bone mass and increased fracture risk. It has been shown that the postprandial suppression of bone resorption in patients with overt diabetes is significantly attenuated, suggesting an additional contributing factor in the deterioration of bone quality and bone mass observed in these patients [20] .…”

“…Postprandial suppression of bone resorption has been studied in diseases that affect bone metabolism through different pathogenetic mechanisms, such as type 2 diabetes mellitus [20] and thyroid diseases [21] . The effect of inflammatory bowel diseases that disturb both bone metabolism and the secretion of gut hormones [22] is currently unknown.…”

Biomarkers of Bone Turnover: Potential, Challenges and Pitfalls from the Laboratory Point of view

“…Postprandial suppression of bone resorption is considered one of the main contributors in the circadian rhythm of bone turnover markers. Accordingly, after oral glucose load, a reduction was observed for BTM, especially CTX (46.9% for β-CTX, 7.9% for P1NP, and 8% for OC) [12].…”

Incretins and bone: Evolving concepts in nutrient-dependent regulation of bone turnover

“…Two recent studies have investigated this phenomenon in patients with type 2 diabetes mellitus, 16 thyroid diseases and beta-thalassemia major, 17 all conditions that are very often complicated with low bone mass and increased fracture risk. It has been shown that the suppression of postprandial bone resorption is attenuated in patients with overt diabetes but not in those with impaired glucose tolerance (IGT), suggesting an additional contributing factor in the deterioration of bone quality and bone mass seen in diabetes.…”