Good long-term glycemic compensation is associated with better trabecular bone score in postmenopausal women with type 2 diabetes
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
31842578
DOI
10.33549/physiolres.934304
PII: 934304
Knihovny.cz E-resources
- MeSH
- Diabetes Mellitus, Type 2 blood drug therapy pathology MeSH
- Glycated Hemoglobin metabolism MeSH
- Hypoglycemic Agents pharmacology therapeutic use MeSH
- Drug Therapy, Combination MeSH
- Bone Density * MeSH
- Middle Aged MeSH
- Humans MeSH
- Metformin pharmacology therapeutic use MeSH
- Postmenopause MeSH
- Cross-Sectional Studies MeSH
- Sitagliptin Phosphate pharmacology therapeutic use MeSH
- Cancellous Bone drug effects pathology MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Glycated Hemoglobin A MeSH
- hemoglobin A1c protein, human MeSH Browser
- Hypoglycemic Agents MeSH
- Metformin MeSH
- Sitagliptin Phosphate MeSH
Osteoporosis is an increasingly widespread disease, as well as diabetes mellitus. It is now accepted that osteoporotic fractures are a serious co-morbidity and complication of diabetes. Despite of good bone mineral density in Type 2 Diabetes (T2DM) patients is the fracture risk elevated. It is due to reduced bone quality. To determine the effect of glycemic compensation on bone density and trabecular bone score (TBS) in T2DM. We analyzed a cohort of 105 postmenopausal women with T2DM. For all patients, central bone density (spinal and lumbar spine) was tested by DXA methodology, glycemic control parameters were assessed, and anthropometric parameters were measured. Bone quality was analyzed using TBS software. The results were statistically processed. Good glycemic compensation with glycated hemoglobin (A1c) value <7.0 % DCCT did not lead to BMD changes in patients with T2DM. However, patients with HbA1c <7 % DCCT had significantly better TBS (1.254±0.148 vs. 1.166±0.094, p=0.01). There was a negative correlation between TBS and glycated hemoglobin (r= -0,112, p<0.05) with glycemic fasting (r= -0.117, p<0.05). The optimal effect on TBS is achieved when all three markers of glycemic compensation (glycated hemoglobin, fasting plasma glucose and postprandial glycemia) are in optimal range. By using ROC curves glycated hemoglobin has the most significant effect on TBS. Optimal glycemic compensation, evaluated by glycated hemoglobin, does not lead to changes in BMD but has a beneficial effect on TBS in T2DM. Good glycemic control is required also for reduction of the risk of osteoporosis and osteoporotic fractures.
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