Pathophysiology of diabetic tendinopathy: an experimental study using type 2 diabetes rat.

Research Project

Project/Area Number	25560270
Research Category	Grant-in-Aid for Challenging Exploratory Research
Allocation Type	Multi-year Fund
Research Field	Rehabilitation science/Welfare engineering
Research Institution	Aino University
Principal Investigator	YOKOTA ATSUSHI 藍野大学, 再生医療研究所, 客員研究員 (10449564)
Project Period (FY)	2013-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000) Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000) Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords	糖尿病 / 腱障害 / ラット / 腱板 / 糖化最終生成物（AGEs） / 運動 / AGE受容体（RAGE) / 糖化最終生成物(AGEs) / AGE受容体(RAGE) / リハビリテーション / 自然発症糖尿病ラット / エクササイズ
Outline of Final Research Achievements	Although the glycation due to accumulation of advanced glycation end products (AGEs) and the interaction between AGEs and the receptors for AGEs (RAGE) appears to be the major cause of diabetic complications, the pathophysiology of diabetic tendinopathy has not been elucidated. Furthermore, the effect of exercise on diabetic tendon is still unknown. Therefore, we utilized the SDT fatty rat, a novel rat model which mimics type 2 diabetes mellitus, to analyze the expression of AGEs and RAGE in the supraspinatus tendon. Histologically, the expression of pentosidine, one of the types of AGEs, and RAGE was increased in the caging SDT Fatty rat. After 16 weeks of exercise by the treadmill, the gene expression of RAGE decreased to 50% compared to that of the caging SDT fatty rats. Those results indicate that one of the primary pathophysiology of the diabetic tendinopathy is the accumulation of pentosidine and RAGE, and that exercise seems to have a prophylactic effect against this disorder.