Glucosamine induces autophagy via an mTOR-independent pathway |
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Authors: | Tomoya Shintani Toshihiko Katoh Yoshiharu Matahira Akira Kakizuka Kenji Yamamoto Hisashi Ashida |
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Affiliation: | a Laboratory of Molecular Biology of Bioresponse, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan b Yaizu Suisankagaku Industry Co., Ltd., Yaizu, Shizuoka 425-8570, Japan c Laboratory of Functional Biology, Graduate School of Biostudies, Kyoto University & Solution Oriented Research for Science and Technology (JST), Kyoto 606-8501, Japan d Ichinoseki National College of Technology, Ichinoseki, Iwate 021-8511, Japan e Laboratory of Molecular Microbiology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan |
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Abstract: | Autophagy is a cellular process that nonspecifically degrades cytosolic components and is involved in many cellular responses. We found that amino sugars with a free amino group such as glucosamine, galactosamine and mannosamine induced autophagy via an mTOR-independent pathway. Glucosamine-induced autophagy at concentrations of at least 500 μM to over 40 mM. In the presence of 40 mM glucosamine, autophagy induction was initiated at 6 h and reached a plateau at 36 h. Glucosamine-induced autophagy could remove accumulated ubiquitin-conjugated proteins as well as 79-glutamine repeats. Therefore, orally administered glucosamine could contribute to the prevention of neurodegenerative diseases and promotion of antiaging effects. |
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Keywords: | Autophagy Chitin Chitosan Glucosamine Hexosamine Polyglutamine disease |
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