Endocrine Functions of Bone Are Suppressed by Orally Administered Glucose Regardless of Bodyweight

Bone is a target for diabetic complications, but the impact of metabolic changes on bone metabolism is less understood. Bones participate in energy metabolism by via secreted osteokines. Glucose ingestion reduces bone resorption, but the effects on osteokines remain unknown. Further, it is not known whether the response is altered in obesity. The objective of the study was to compare responses in circulating levels of osteokines to glucose ingestion between participants with normal weight (BMI < 26 kg/m², n = 22) and obesity (BMI > 28 kg/m², n = 27) (age = 21-54 yr).

C-terminal telopeptide of collagen I (b-CTX-I), total osteocalcin (OC), sclerostin, fibroblast growth-factor 23 (cFGF23), uncarboxylated OC, and lipocalin 2 (LCN2) at baseline and after 2 h oral glucose tolerance test (OGTT).

OGTT resulted in a significant decrease in bone resorption, median decrease in b-CTX-I was 42% (p < 0.0001) in both groups. Osteokine levels were modestly but statistically significantly decreased, OC decreased by 11% (p < 0.0001) and FGF23 by 14% (p = 0.007) in both groups, while uncarboxylated OC decreased by 1.2% (p < 0.0001) and sclerostin by 7.8% (p = 0.032) only in participants with obesity. Although the differences in responses between the groups were not statistically significant, we observed a tendency for less pronounced effect on b-CTX-I (p = 0.052) and a greater effect on OC (p = 0.051) in participants with obesity compared to normal weight.

Osteokines respond rapidly to oral glucose regardless of body weight. Orally-administered glucose affects not only bone turnover but can also suppress bone endocrine functions. Furthermore, obesity may influence the effect of oral glucose on circulating levels of bone turnover markers.