The role of bone marrow and visceral fat on bone mineral density and fracture occurrence in type 2 diabetes mellitus

Abstract

recently, fat tissue was considered a site with low metabolic activity hardly contributing to the regulation of energy homeostasis. Similarly, bone tissue was associated with mechanical support and accepted as a mine of minerals. In the last decades, evidence indicates an important interactive role between fat and bone tissues in the energetic and mineral regulation. These new network is remarkable; osteoblasts and adipocytes share a common progenitor marrow stem cells. Adiponectin and leptin, two adipokines released by the fat tissue, influence the energetic homeostasis and bone metabolism. On the other hand, peptides synthesized by osteoblasts, e.g. osteocalcin, may increase the sensitivity to as well as the release of insulin. In this scenario, recently emerges a growing interest on the study of the interrelationship between not only energetic and bone metabolism, but also between diabetes mellitus and osteoporosis, in view that these disorders have a great impact in public health. The current proposal was designed to evaluate several mechanisms involved with the occurrence of bone disease in diabetes mellitus type 2. We also intend to verify the association of biochemical parameters with qualitative/quantitative changes in bone tissue of patients harboring type 2 diabetes. Data obtained in diabetic patients will be analyzed in comparison with control subjects.