Abstract

ObjectiveIncreasing evidence suggests that osteocalcin (OC), a marker of bone formation, plays an important role in glucose homoeostasis. Few studies have investigated the relationship between OC levels in gestational diabetes mellitus (GDM) patients and their postpartum glucose metabolism. This study evaluated the relationship between OC levels in late pregnancy, their longitudinal changes, and postpartum glucose metabolism among GDM patients.MeasuresSerum OC was measured in late pregnancy and the postpartum period for 721 GDM patients. All patients underwent a 75-g oral glucose tolerance test (OGTT) at 6–8 weeks postpartum. According to postpartum OGTT outcomes, patients were categorized into abnormal glucose metabolism (AGM) (n=255) and normal glucose tolerance (NGT) groups (n=466). Glucose metabolism-related indices were measured and calculated. Logistic regression analysis and linear mixed-effects model were used to assess the association between OC and postpartum AGM.ResultsIn late pregnancy, OC levels were lower in the AGM group than in the NGT group (13.93 ± 6.90 vs 15.33 ± 7.63 ng/ml, P=0.015). After delivery, OC levels increased in both groups. However, OC levels remained lower in the AGM group than in the NGT group (23.48 ± 7.84 vs 25.65 ± 8.37 ng/ml, P=0.001). Higher OC levels in late pregnancy were associated with decreased risk of progressing to postpartum AGM (OR:0.96, 95%CI:0.94–0.99). Linear mixed-effects analysis showed that postpartum AGM patients exhibited consistently lower OC levels than NGT group from late pregnancy to the postpartum period after adjustment for cofactors (β=-1.70, 95% CI: -2.78– -0.62). ConclusionsIn GDM patients, consistently low levels of OC from late pregnancy to postpartum were associated with increased postpartum AGM risk. The increase in serum OC may act as a protective factor to curb the progression of AGM at postpartum for GDM patients.

Highlights

  • Bone has been identified as an endocrine organ involved in energy metabolism through the secretion of specific hormones [1, 2]

  • According to the results of the postpartum OGTT, 255 individuals were diagnosed with Abnormal glucose metabolism (AGM), of whom 221 had impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) and 34 had diabetes

  • Postpartum FBG, 2-h postprandial glucose (2h-PG), 2h-INS, total cholesterol (TC), TGs and lowdensity lipoprotein cholesterol (LDL-C) were significantly higher in the AGM group

Read more

Summary

Introduction

Bone has been identified as an endocrine organ involved in energy metabolism through the secretion of specific hormones [1, 2]. Osteocalcin (OC), a small noncollagenous protein of 49 amino acids that is exclusively secreted by osteoblasts, participates in bone remodeling and calcium homeostasis. Accumulating evidence shows that OC is vital in the crosstalk between bone remodeling and energy metabolism. Extensive animal studies have shown that OC stimulates insulin secretion directly by exerting an effect on pancreatic b-cell and indirectly via the secretion of glucagon-like peptide (GLP-1) by enteroendocrine L cells leading to improved insulin sensitivity [8, 9]. Serum OC was reported to be decreased in patients with type 2 diabetes compared to the levels in nondiabetic controls; inversely associated with blood glucose levels, HbA1c, BMI and insulin resistance; and positively associated with insulin secretion and insulin sensitivity [7, 11, 12]

Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.