Akademik Veri Yönetim Sistemi
Israel Journal of Veterinary Medicine, cilt.68, sa.3, ss.158-166, 2013 (SCI-Expanded)
This randomized experimental study was conducted to determine the effect of melatonin on bone healing processes in diabetic rats with bone defects. Adult male Sprague Dawley rats (n = 64) were divided into diabetic and control groups. The diabetic group was administered with streptozotocin (60 mg/kg BW, (intraperi-toneally) I.P.), whereas the control group was administered with saline containing 6% ethanol intraperito-neally. Defects were created in the left tibias, and rats were then administered with either saline or melatonin (10 mg/kg BW, I.P.) for 21 or 42 days. Overall, the diabetic rats had significantly higher serum glucose concentrations than the control rats (462 vs. 118 mg/dl; P<0.0001). Melatonin administration increased serum glucose by 5% in the control groups and decreased it by 43% in the diabetic groups (P<0.0001). Serum melatonin concentrations in the control rats were lower than in the diabetic rats (666 vs. 745 pmol/L; P<0.006). Melatonin administration increased serum melatonin concentrations to a similar extent in both groups (by 15%). Diabetes was associated with pathologies (degranulation, vacuolization, degeneration, and necrosis) in pancreatic β cells and aggravated inflammation indicators (P<0.0001 for all). Melatonin administration considerably decreased the number of rats with pancreatic β cell pathologies (63%) and depressed inflammation indicators (from P<0.004 to P<0.0008). Melatonin administration increased osteogenesis indicators (collagen, cartilage, and osteocyte intensities) (2.0 vs. 1.0; P<0.04) and numerically decreased inflammation indicators (macrophage, lymphocyte, and polymorph nuclear leukocyte) (1.0 vs. 2.0) at a greater extent in the diabetic rats than in the control rats. In conclusion, postoperative administration of melatonin supports bone healing in diabetic rats apparently through alleviating pancreatic cytopathology and hyperglycemia.