Chinese Journal of Tissue Engineering Research ›› 2016, Vol. 20 ›› Issue (40): 6041-6047.doi: 10.3969/j.issn.2095-4344.2016.40.017

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Establishing a rat model of type 2 diabetes: its bone metabolism level

Zhang Yan1, Yang Qiu-ping2, Zhao Yan1, Zhao Yu-mei1, Tan Hong1, Du Si-cheng1   

  1. 1Department of Diabetes, 2Department of Cadre’s Ward, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
  • Revised:2016-07-14 Online:2016-09-30 Published:2016-09-30
  • Contact: Yang Qiu-ping, Master, Chief physician, Professor, Department of Cadre’s Ward, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
  • About author:Zhang Yan, Studying for master’s degree, Department of Diabetes, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
  • Supported by:

    the Joint Special for Applied Basic Research of Yunnan Provincial Science and Technology Department-Kunming Medical University, No. 2013FZ270; the Innovation Foundation for the Postgraduate in Kunming Medical University, No. 2014N04

Abstract:

BACKGROUND: Diabetes mellitus can give rise to bone metabolic disorders that may involve long-term hyperglycemia, hypoglycemic agents, diet control, estrogen, insulin-like growth factor, leptin, body mass, sex and age.

OBJECTIVE: To establish type 2 diabetic rat models, and to explore the influence of type 2 diabetes on bone metabolism.
METHODS: High-fat and high-glucose diets combining with 35 mg/kg streptozotocin were used to induce type 2 diabetic model in seven male Sprague-Dawley rats (diabetic group). Thirteen rats in control group were given intraperitoneal injection of the same amount of citric acid and sodium citrate buffer. At 4 weeks after modeling, the bone density of rats was serum detected by dual-energy X-ray, levels of fasting blood-glucose, cholesterol, triacylglycerol, serum calcium, phosphate, alkaline phosphatase, fasting insulin, osteocalcin and C-terminal telopeptide-I were measured, and morphology of bone was observed.
RESULTS AND CONCLUSION: Compared with control group, (1) the rat body mass and fasting blood-glucose kept on an overt rise in the diabetic group (P < 0.05); (2) levels of cholesterol, triacylglycerol, fasting insulin and alkaline phosphatase, as well as insulin resistance index were significantly increased, but insulin sensitivity index was significantly decreased in the diabetic group (P < 0.05). (3) There were no significant differences in the levels of serum calcium, phosphate, alkaline phosphatase, osteocalcin and C-terminal telopeptide-I between two groups (P > 0.05). (4) In the diabetic group, thinner and sparse bone trabeculae were split presenting more free broken ends; (5) the bone density in lumbar spine, double femoral, pelvic and thoracolumbar spine were all significantly decreased (P < 0.05). (6) In conclusion, the type 2 diabetic rat model can be successfully induced by 5-week feeding high-fat and high-glucose diets combining with intraperitoneal injection of 35 mg/kg streptozotocin; these mode rats hold some characters, such as hyperglycemia, dyslipidemia, insulin resistance, diminished bone density, and accelerated bone resorption.

 

Key words: Diabetes Mellitus, Type 2, Osteoporosis, Bone Density, Tissue Engineering

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