Obesity Effects on Bone Femur Tissue of Animals Subjected to Obesity through High-fat Diet

Abstract

Introduction: Adipose corporal tissue accumulation may cause alterations in the bone metabolism and might influence its properties. However, there are still many controversies, in addition to how the adipose tissue can cause these changes. Aims: To evaluate the femur bone tissue behavior of animals submitted to obesity through cafeteria diet. Place of Study: The Ethics Committee on Animal Experiments and Practical Classes (CEEAAP) of UNIOESTE has approved the project, which was developed at the same university. Methodology: It was used twenty-four 8-week-old male Wistar rats, which were obtained at UNIOESTE’s central vivarium and kept in the Endocrine Physiology and Metabolism Lab of this institution. The animals were divided in: CONTROL group (CG) that received a standard diet and OBESE group (OG) that underwent a high-fat diet, during 28 weeks. We analyzed the obesity parameters, such as body weight and Lee index and femur bone properties like the quantity of osteocytes, the thickness of the cortical bone mass and the epiphyseal line’s thickness. All data were analyzed and evaluated using the Student-T Test (p<0.01).  Results: The results pointed that the animals that underwent a high fat diet became obese (OG= 624.00±4.00 g vs CG= 466.00±1.50 g). The obese animals presented a statistically significant (p< 0.01) decrease of all analyzed bone parameters, when compared to the non-obese animals, including the amount of osteocytes (OG= 27.20±0.90 vs CG= 30.30±0.70), the thickness of the epiphyseal line (OG= 171.70±0.92 µm vs CG= 175.50±1.07 µm) and the thickness of femur cortical bone mass (OG= 434.10±2.03 µm vs CG= 495.50±2.55 µm). Conclusions: The obesity had negative influences on the femur bone tissue of the animals that received a high-fat diet, due to a finding of a decrease on all bone parameters analyzed. We could highlight, too, that the applied cafeteria diet was effective to induce obesities in the animals.