Abstract
Bone is an endocrine organ involved in modulating glucose homeostasis. The role of the bone formation marker osteocalcin (OCN) in predicting diabetes was reported, but with conflicting results. No study has explored the association between baseline bone resorption activity and incident diabetes or prediabetes during follow-up. Our objective was to examine the relationship between the baseline bone resorption marker crosslinked C-telopeptide of type I collagen (CTX) and glycemic dysregulation after 4 years. This longitudinal study was conducted in a university teaching hospital. A total of 195 normal glucose tolerant (NGT) women at baseline were invited for follow-up. The incidence of diabetes and prediabetes (collectively defined as dysglycemia) was recorded. A total of 128 individuals completed the 4-year study. The overall conversion rate from NGT to dysglycemia was 31.3%. The incidence of dysglycemia was lowest in the middle tertile [16.3% (95% confidence interval (CI), 6.8%–30.7%)] compared with the lower [31.0% (95% CI, 17.2%–46.1%)] and upper [46.5% (95% CI, 31.2%–62.6%)] tertiles of CTX, with a significant difference seen between the middle and upper tertiles (P=0.002 5). After adjusting for multiple confounding variables, the upper tertile of baseline CTX was associated with an increased risk of incident dysglycemia, with an odds ratio of 7.09 (95% CI, 1.73–28.99) when the middle tertile was the reference. Osteoclasts actively regulate glucose homeostasis in a biphasic model that moderately enhanced bone resorption marker CTX at baseline provides protective effects against the deterioration of glucose metabolism, whereas an overactive osteoclastic function contributes to an increased risk of subsequent dysglycemia.
Highlights
Diabetes is a worldwide health problem.[1]
10 years, mounting evidence from mouse models has suggested a promising role of the skeleton in regulating glucose homeostasis, mainly through a bone protein synthesized by osteoblasts called osteocalcin (OCN), which can stimulate insulin release from β cells and improve insulin sensitivity.[6,7,8,9]
Previous mouse studies clearly indicated that the formation of the metabolically active form of OCN, which can augment insulin release from pancreatic β cells and improve insulin resistance, relies on the acidic bone microenvironment provided by enhanced osteoclastic activity.[14,18,19]
Summary
Diabetes is a worldwide health problem.[1]. Epidemiological studies have reported a prevalence of prediabetes as high as 30%–50%.2–3 It was estimated that 20%–25% of normal glucose tolerant (NGT) subjects will develop prediabetes and diabetes in 10 years;[4] there is an urgent need to identify subjects at high risk of developing prediabetes and diabetes. Diabetes is a worldwide health problem.[1] Epidemiological studies have reported a prevalence of prediabetes as high as 30%–50%.2–3. It was estimated that 20%–25% of normal glucose tolerant (NGT) subjects will develop prediabetes and diabetes in 10 years;[4] there is an urgent need to identify subjects at high risk of developing prediabetes and diabetes. Bone is an ever-changing organ that actively participates in the regulation of energy homeostasis.[5] In the last. 10 years, mounting evidence from mouse models has suggested a promising role of the skeleton in regulating glucose homeostasis, mainly through a bone protein synthesized by osteoblasts called osteocalcin (OCN), which can stimulate insulin release from β cells and improve insulin sensitivity.[6,7,8,9] most, but not all, human crosssectional investigations lend support to the negative associations between the bone formation marker OCN and fasting plasma glucose (FPG) and glycated hemoglobin (HbA1c),[10] data from a limited number of longitudinal human studies are not consistent.[11,12]
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