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Effects of insulin therapy on fracture healing and expression of VEGF in diabetic rats
Da-Wei Wang, Shun-Lei Du, Ming-Tao Xu, Yi-Ting Lu, Zhan-Chao Wang, Le-Xin Wang
Language English Country Czech Republic
Document type Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 2003 to 2013
Freely Accessible Science Journals
from 2003 to 2013
ROAD: Directory of Open Access Scholarly Resources
from 2002
- MeSH
- Biomechanical Phenomena MeSH
- Chondrocytes pathology drug effects MeSH
- Diabetes Mellitus, Experimental drug therapy complications physiopathology MeSH
- Femur pathology radiography drug effects MeSH
- Femoral Fractures * drug therapy physiopathology pathology radiography MeSH
- Wound Healing drug effects MeSH
- Immunohistochemistry MeSH
- Insulin * therapeutic use MeSH
- Bony Callus physiopathology drug effects MeSH
- Disease Models, Animal MeSH
- Rats, Wistar MeSH
- Case-Control Studies MeSH
- Vascular Endothelial Growth Factors * analysis drug effects MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
This study was designed to investigate effects of insulin on fracture healing and expression of vascular endothelial growth factor (VEGF) in diabetic rats. Wister rats were randomly divided into diabetic control (n=66), diabetic insulin (=66) and non-diabetic control group (n=66). Diabetes was established by peritoneal injection of alloxan. Tibia fracture was surgically created and was allowed to heal. Radiological and biomechanical examinations were performed on the healing tibia. Immuohistochemistry was used to assess VEGF expression in the healing fracture tissues. Cortical reconstruction of the fracture sites in non-diabetic control and diabetic insulin groups was more rapid than in diabetic control group within 6 weeks of the fracture. Mechanical strength of the affected tibia in the diabetic insulin and non-diabetic control group was superior to diabetic control group. Histological examination of the fracture sites revealed a delay in chondrocyte maturation and hypertrophy in diabetic control group. VEGF expression was widely distributed in fracture sites within the first 4 weeks in control and diabetic insulin treatment group. However VEGF expression in the callus and periosteum in diabetic control group was much less than in diabetic insulin or non-diabetic control group. In conclusion, diabetes delays fracture healing and adversely affects callus formation with a reduced VEGF expression at the fracture sites. Insulin therapy improves fracture healing in diabetes rats, possibly through enhancing VEGF expression in the fractured bones.
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Literatura
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- $a Wang, Da-Wei $u Department of Orthopedic Surgery, Liaocheng People's Hospital and Liaocheng Clinical School of Taishan Medical University, Liaocheng, China; School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, Australia
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- $a This study was designed to investigate effects of insulin on fracture healing and expression of vascular endothelial growth factor (VEGF) in diabetic rats. Wister rats were randomly divided into diabetic control (n=66), diabetic insulin (=66) and non-diabetic control group (n=66). Diabetes was established by peritoneal injection of alloxan. Tibia fracture was surgically created and was allowed to heal. Radiological and biomechanical examinations were performed on the healing tibia. Immuohistochemistry was used to assess VEGF expression in the healing fracture tissues. Cortical reconstruction of the fracture sites in non-diabetic control and diabetic insulin groups was more rapid than in diabetic control group within 6 weeks of the fracture. Mechanical strength of the affected tibia in the diabetic insulin and non-diabetic control group was superior to diabetic control group. Histological examination of the fracture sites revealed a delay in chondrocyte maturation and hypertrophy in diabetic control group. VEGF expression was widely distributed in fracture sites within the first 4 weeks in control and diabetic insulin treatment group. However VEGF expression in the callus and periosteum in diabetic control group was much less than in diabetic insulin or non-diabetic control group. In conclusion, diabetes delays fracture healing and adversely affects callus formation with a reduced VEGF expression at the fracture sites. Insulin therapy improves fracture healing in diabetes rats, possibly through enhancing VEGF expression in the fractured bones.
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