INCREASING SERUM OSTEOCALCIN AFTER GLYCEMIC CONTROL IN DIABETIC MEN

Citation
S. Sayinalp et al., INCREASING SERUM OSTEOCALCIN AFTER GLYCEMIC CONTROL IN DIABETIC MEN, Calcified tissue international, 57(6), 1995, pp. 422-425
Citations number
32
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0171967X
Volume
57
Issue
6
Year of publication
1995
Pages
422 - 425
Database
ISI
SICI code
0171-967X(1995)57:6<422:ISOAGC>2.0.ZU;2-Z
Abstract
The pathogenesis of diabetic osteopenia is unclear. The markers of bon e metabolism may show some changes in diabetic patients, In this study , we investigated the effect of glycemic control on serum osteocalcin level and urinary hydroxyproline excretion and the relations of these markers to duration of diabetes, C-peptide status, and body mass index . Twenty-seven men with poorly controlled diabetes mellitus (DM) (HbA1 > 9%, fasting plasma glucose > 7.8 mmol/liter) between ages 25 and 60 years (means +/- SD 46.6 +/- 10.4) were included in the study. Durati on of diabetes was 5.8 +/- 4.7 years, body mass index (BMI) was 25.9 /- 3.5 kg/m(2), and fasting C-peptide was 2.33 (1.05-3.21) mu g/liter. None of the patients had a disease or were treated with drugs that wo uld interfer with calcium or phosphate metabolism and/or bone structur e. They were free from chronic diabetic complications. Of these patien ts, 11 were lost to follow-up before metabolic control was achieved. T he remaining 16 patients obtained good glycemic control (HbA1 < 8.3%, fasting plasma glucose < 7.8 mmol/liter) and completed the study. Seru m osteocalcin level and urinary hydroxyproline excretion were determin ed before and after glycemic control. Urinary hydroxyproline excretion was not significantly changed by glycemic control [17.8 (7.1-23.2) ve rsus 18.1 (10.9-28.1) mg/m(2) day, P > 0.05]. However, serum osteocalc in level was significantly elevated (5.04 +/- 1.43 versus 4.17 +/- 1.8 3 mu g/liter, P = 0.04). We found no correlation among fasting plasma glucose, HbA1, and fasting serum C-peptide levels with urinary hydroxy proline excretion. There was also no correlation between serum osteoca lcin and fasting plasma glucose or serum C-peptide, but HbA1 was negat ively correlated with serum osteocalcin (P = 0.01). No correlation was found between DM duration and BMI in the patients with serum osteocal cin level and urinary hydroxyproline excretion. To eliminate the possi ble effect of exogenous insulin on bone metabolism, the correlation an alysis between the markers and C-peptide was further repeated in oral agents-treated patients. Serum C-peptide was not correlated to serum o steocalcin or urinary hydroxyproline in this subgroup of patients. Kno wing that serum osteocalcin is a marker of bone formation, we conclude d that osteoblast function may improve by glycemic control in diabetic patients; this may be due to correction of metabolic abnormalities as sociated with insulinopenia.