Low Osteocalcin Linked to Glucocorticoid-Induced Diabetes

September 16, 2020

Low levels of osteocalcin are associated with an increased risk of diabetes in patients treated with glucocorticoids, according to a study presented on Sept. 11 at the American Society for Bone and Mineral Research (ASBMR) annual meeting which wrapped this week as a virtual meeting.

Low levels of osteocalcin are associated with an increased risk of diabetes in patients treated with glucocorticoids, according to a study presented on Sept. 11 at the American Society for Bone and Mineral Research (ASBMR) annual meeting which wrapped this week as a virtual meeting.

Osteocalcin is a marker of bone turnover. It is stimulated by 1,25 dihydroxy vitamin D and depends on vitamin K. Treatment with glucocorticoids is associated with impaired osteoblast function and decreased osteocalcin levels and also with the development of glucocorticoid-induced diabetes mellitus. However, it is not clear whether decreased osteocalcin levels in patients treated with glucocorticoids contribute to glucocorticoid-induced diabetes mellitus.

In this study, Pilar Peris, M.D., of the Hospital Clinic in the University of Barcelona, found that osteocalcin may be useful as a biomarker for identifying subjects who are at risk of developing diabetes related to glucocorticoid treatment.

Dr. Peris and colleagues analyzed whether osteocalcin levels in 127 patients on glucocorticoid treatment were associated with the presence of glucocorticoid-induced diabetes mellitus. The patients had a mean age of 62 years, 63 percent were women and they were all taking glucocorticoids (≥5mg/day,>3 months) for autoimmune diseases.

Of the patients, 17.3 percent had glucocorticoid-induced diabetes mellitus. These patients were older than those without diabetes (70.5 versus 59.6 years, p=0.001) and had a higher body mass index (30 versus 26, p=0.002). No differences were found between patients with diabetes and patients without diabetes in glucocorticoid dose, disease duration or in the presence of vertebral fractures.

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Patients with diabetes had lower levels of the bone formation markers osteocalcin (7.57 versus 11.56, p<0.001) and procollagen type I N propeptide (PINP: 21.48 versus 28.39, p=0.0048) than patients without diabetes, but similar bone alkaline phosphatase (BAP) values. Patients with diabetes also had lower levels of the bone resorption markers urinary N-terminal telopeptide (NTX: 24.91 versus 31.7, p=0.036) and serum carboxy-terminal collagen crosslinks (CTX: 0.2 versus 0.3, p=0.0016) than patients without diabetes.

The best cut-offs of each bone marker for the presence of glucocorticoid-induced diabetes mellitus were estimated as follows: <9.25ng/mL for OC, <24ng/mL for PINP, <27.5nMol/mM for NTX and <0.25ng/mL for CTX. Further analysis showed that OC <9.25ng/mL was the only bone marker related to the presence of glucocorticoid-induced diabetes mellitus (OR 6.1; CI 95% 1.87-19.89; p=0.001).

“Decreased osteocalcin levels in glucocorticoid-treated patients are associated with an increased risk of glucocorticoid-induced diabetes mellitus, a finding that was not observed with other bone turnover markers,” the authors wrote. The results further confirm “the involvement of osteocalcin in the glucose homeostasis regulation in this entity.”

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REFERENCE

[P-624] Low Serum Osteocalcin Levels are Associated with the Presence of Diabetes Mellitus in Glucocorticoid Treated Patients. Pilar Peris. September 11. ASMBR 2020 Annual Meeting Virtual Event.