ORAL ADMINISTRATION OF ALLULOSE ATTENUATES CISPLATIN-INDUCED AKI VIA GLP-1 RELEASE

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Abstract Title *

ORAL ADMINISTRATION OF ALLULOSE ATTENUATES CISPLATIN-INDUCED AKI VIA GLP-1 RELEASE

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Co-author 1

Jumpei Yamashita jyamashita0502@gmail.com The University of Tokyo Division of Nephrology and Endocrinology Tokyo Japan *

Co-author 2

Wei Zou 3512283453@qq.com The University of Tokyo Division of Nephrology and Endocrinology Tokyo Japan -

Co-author 3

Yusaku Iwasaki ysk-iwasaki@kpu.ac.jp Kyoto Prefectural University Laboratory of Animal Science Kyoto Japan -

Co-author 4

Masaomi Nangaku mnangaku@m.u-tokyo.ac.jp The University of Tokyo Division of Nephrology and Endocrinology Tokyo Japan -

Co-author 5

Shinji Tanaka shitanaka@m.u-tokyo.ac.jp The University of Tokyo Division of Nephrology and Endocrinology Tokyo Japan -

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Introduction

About 10% of hospitalized patients and 50% of intensive care unit patients suffer from acute kidney injury (AKI). Besides, it sometimes leads to chronic/end-stage kidney disease. But there is no specific treatment for AKI. Therefore, it is essential to find the new treatment strategy for AKI. Recently, several studies demonstrated that oral administration of D-allulose (rare sugar) induced glucagon-like peptide-1 (GLP-1) release to activate vagal afferent signaling and reduce food intake in mice. On the other hand, we previously demonstrated that the vagal afferents-C1 neurons-sympathetic nervous system-splenic nerve-spleen-kidney axis played an important role for kidney protection. Taken together, we hypothesized that D-allulose has renoprotective effect via GLP-1 release and vagal afferent stimulation.

Methods

We used three mouse AKI models (ischemia reperfusion injury, cisplatin administration, and lipopolysaccharide administration) for evaluating renoprotective effect of orally administrated allulose. In addition, we used Glp1r global knock out mice and exendin (9-39), which is GLP-1 antagonist, to demonstrate that GLP-1 signaling is essential for the renoprotective effect of allulose. D-allulose was kindly provided by Matsutani Chemical Industry Company.

Results

Orally administered allulose had renoprotective effect only in the cisplatin-induced AKI model for wild type mice(C57BL/6J). However, the protective effect was not observed with subcutaneous allulose administration or oral glucose administration. Moreover, the renoprotection was partially canceled by exendin (9-39) administration and completely canceled in Glp1r global knock out mice.

Conclusion

Oral administration of allulose has renoprotective effect for cisplatin-induced AKI probably through the release of GLP-1. Further studies including vagal afferent ablation will be needed to elucidate the precise mechanism.

Kewords