Diabetoporosis or Diabetic Osteodystrophy
Issue: Supplement to issue 3/2017
Author: Ivanova, Anna-Maria Borissova
“Sofiamed” University Hospital,
Medical Faculty, Sofia University
Abstract:
Despite the fact that subjects with T2DM have higher bone mineral density (BMD) than nondia-betic population, there is an increasing evidence that they present up to two fold increased risk of fractures. The main explanation of this fact is the decreased bone quality in diabetes. The high level of the transcription factor PPARγ promotes accu-mulation of adipocytes in the bone marrow, and in the same time decreases the differentiation of stem cells to osteoblasts. In addition, the high PPARγ controls glucose metabolism from osteo-cytes. The inflammatory factors (interleukins and adipokines) may have influence on both insulin resistance and bone turnover. Bone-derived mole-cules − undecarboxylated osteocalcin and RANKL, have their influence in the regulation of glucose metabolism. Hypoglycaemias, visual disturbances, and diabetic neuropathy increase the chance of falls, that could be an important risk factor for fractures. Some antidiabetic drugs, such as PPARγ activators (glitazones), may exert a negative impact on the frac-ture risk despite of the better glucose control.
Bone changes in the patients with T1DM are related to the deficiency of the anabolic hormone insulin, frequent ketoacidoses, loss of P++ through polyuria, decreased synthesis of proteins including bone collagen. All the above-mentioned factors related to diabetes have also their important role.
Recently, it was established that treatment with GLP-1 receptor agonists (GLP-1 RA) resulted in improvement of bone metabolism and a signifi-cant increase in bone mass. The GLP-1 RA mediat-ed osteogenic action is exerted through GLP-1 receptors, mainly expressed on the bone marrow stromal cells (BMSC). Thus, GLP-1 RA promoted BMSC osteoblast differentiation and inhibited their differentiation into adipocytes, leading to anabolic bone formation and prevention or amelioration of osteoporosis.
Key words: diabetes mellitus, bone mineral density, osteoporosis, osteocalcin, GLP-1 receptor agonists
