Alteration of glycan-related gene expressions by the supplementation of products derived from cartilage

Research Project

Project/Area Number	26350153
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Eating habits
Research Institution	University of Niigata Prefecture
Principal Investigator	KAMIYAMA Shin 新潟県立大学, 人間生活学部, 准教授 (70525401)
Project Period (FY)	2014-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000) Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Keywords	糖鎖 / 軟骨 / コラーゲンペプチド / 関節リウマチ / グリコサミノグリカン / グルコサミン / 関節炎 / リウマチ / コラーゲン
Outline of Final Research Achievements	The present study revealed that the two typical collagen dipeptides, prolyl-hydroxyproline (Pro-Hyp) and hydroxyprolyl-glycine (Hyp-Gly), increase the expression of type II collagen and chondroitin sulfate proteoglycan and promote early chondrogenesis in ATDC5 cells. Further, chicken type II collagen peptides and glucosamine had synergistic effects on the arthritis score and synovial inflammation in SKG mice. In contrast, administration of chicken type I collagen peptides or its constituent amino acids worsened collagen-induced inflammatory arthritis in DBA/1J mice. These findings indicate that supplementation of type II collagen peptides may have beneficial effects on rheumatoid arthritis via oral tolerance rather than stimulation of chondrogenesis unlike type I collagen peptides.