Abstract
Background: Osteoporosis is a metabolic skeletal disease with low bone mass and bone microarchitectural disorganization. Thiazolidinediones (TZD) increase insulin sensitivity through activation of peroxisome proliferator-activated receptor gamma (PPARγ). One of the most important side effects of this drugs is its effects on bone, especially in postmenopausal women. The purpose of this study was to evaluate the effect of diabetes mellitus (DM), insulin, and TZDs on bone in postmenopausal Wistar rats.
 Methods: Sixteen postmenopausal Wistar rats were divided into four groups: (i) control group, (ii) Streptozotocin-induced DM group without treatment, (iii) Streptozotocin-induced DM group with insulin therapy, and (iv) Streptozotocin-induced DM group receiving rosiglitazone. Pictures of the obtained samples were taken under computer-equipped photo-light microscope, and bone tissue ratios were calculated in an area of 1 mm2. In this area, trabecular thicknesses were measured from six randomly selected regions. In addition, femoral neck regions were determined by measuring the farthest distance.
 Results: Compared to the control group, trabecular thicknesses were decreased in the uncontrolled DM and rosiglitazone groups. In the rosiglitazone-treated group, trabecular thickness was decreased compared to the uncontrolled DM group. The histological examination of the bones showed that uncontrolled DM and rosiglitazone treatment negatively affected the osteoblast and osteocyte activity. Insulin-treated group had a similar histologic examination compared to the control group.
 Conclusion: Our study showed that DM had unfavorable effects on bones, and rosiglitazone further exerts this effect. However, the negative effect of DM may be neutralized with the use of insulin.
 Keywords: diabetes mellitus, bone, osteoporosis, bone histomorphometry, rosiglitazone, insulin, thiazolidinediones
Highlights
It is well-known that there is an increase in bone fragility in patients with type-1 diabetes mellitus (DM) [1, 2]
Gimble et al showed that expression of adipocyte-specific genes and adipocyte count increased with the addition of pioglitazone and rosiglitazone to the cell medium containing bone marrow stromal cells [7]
This study was aimed at clarifying the relationship between DM and the drugs used in the treatment for DM with bone fragility through detailed examinations of the effects of DM, blood glucose (BG) regulation with insulin, and TZDs on the bone
Summary
It is well-known that there is an increase in bone fragility in patients with type-1 diabetes mellitus (DM) [1, 2]. Epidemiological studies have shown that, despite the normal-high bone mineral density (BMD), the risk of fractures increases in type-2 DM patients. Thiazolidinedione (TZD) is an oral antidiabetic drug group that increases insulin sensitivity by activation of peroxisome proliferator-activating receptor gamma (PPARγ). Thiazolidinediones (TZD) increase insulin sensitivity through activation of peroxisome proliferator-activated receptor gamma (PPARγ). The purpose of this study was to evaluate the effect of diabetes mellitus (DM), insulin, and TZDs on bone in postmenopausal Wistar rats. Pictures of the obtained samples were taken under computerequipped photo-light microscope, and bone tissue ratios were calculated in an area of 1 mm2 In this area, trabecular thicknesses were measured from six randomly selected regions. The negative effect of DM may be neutralized with the use of insulin
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