| Project/Area Number |
17K17579
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
Metabolomics
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| Research Institution | Hirosaki University |
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Principal Investigator |
Uchida Chiaki 弘前大学, 医学研究科, 客員研究員 (80791714)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 膵星細胞 / 膵管癌 / 2型糖尿病 / AGEs / ２型糖尿病 / 終末糖化産物 / 膵導管癌 / 膵臓外科学 / エネルギー・糖質代謝異常 |
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| Outline of Final Research Achievements |
Type 2 diabetes is a poor prognostic factor in pancreatic ductal carcinoma, but the detailed mechanism is unknown. This study focused on pancreatic stellate cells and aimed to elucidate the effect of type 2 diabetes on pancreatic ductal caricnoma via pancreatic stellate cells.
We add the AGEs that have increased secretion in type 2 diabetes, to mouse-derived pancreatic stellate cells, and analyzed the activity. We revealed that pancreatic stellate cells with AGEs were more activated. In addition, we observed the surgical specimens, it was clarified that patients with pancreatic ductal carcinoma who had type 2 diabetes had stronger fibrosis around the cancer cells that seem to be derived from pancreatic stellate cells. These findings suggest that type 2 diabetes promotes fibrosis of peri-tumor stroma via pancreatic stellate cells, which may lead to worse prognosis.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、2型糖尿病が膵星細胞を介して膵管癌の悪性度に寄与している機序の一つを明らかにすることができた。この結果から、いまだに予後の最も悪い癌腫の一つである膵管癌の進行、進展の機序の解明につながる可能性がある。また、本研究をさらに発展させることができれば、癌周囲間質の制御を介した膵管癌の新規治療法の開発につながる可能性があると思われる。
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