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SLC7A14 imports GABA to lysosomes and impairs hepatic insulin sensitivity via inhibiting mTORC2

Published:31 January 2023 DOI: 10.1016/j.celrep.2022.111984 PMID: 36640347
Xiaoxue Jiang, Kan Liu, Haizhou Jiang, Hanrui Yin, En-Duo Wang, Hong Cheng, Feixiang Yuan, Fei Xiao, Fenfen Wang, Wei Lu, Bo Peng, Yousheng Shu, Xiaoying Li, Shanghai Chen, Feifan Guo

Abstract

Lysosomal amino acid accumulation is implicated in several diseases, but its role in insulin resistance, the central mechanism to type 2 diabetes and many metabolic diseases, is unclear. In this study, we show the hepatic expression of lysosomal membrane protein solute carrier family 7 member 14 (SLC7A14) is increased in insulin-resistant mice. The promoting effect of SLC7A14 on insulin resistance is demonstrated by loss- and gain-of-function experiments. SLC7A14 is further demonstrated as a transporter resulting in the accumulation of lysosomal γ-aminobutyric acid (GABA), which induces insulin resistance via inhibiting mTOR complex 2 (mTORC2)'s activity. These results establish a causal link between lysosomal amino acids and insulin resistance and suggest that SLC7A14 inhibition may provide a therapeutic strategy in treating insulin resistance-related and GABA-related diseases and may provide insights into the upstream mechanisms for mTORC2, the master regulator in many important processes.

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9-(6-Amino-3-pyridinyl)-1-[3-(trifluoromethyl)phenyl]benzo[h]-1,6-naphthyridin-2(1H)-one 1223001-51-1 C24H15F3N4O 194 suppliers $65.00-$6254.00
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9-(6-Amino-3-pyridinyl)-1-[3-(trifluoromethyl)phenyl]benzo[h]-1,6-naphthyridin-2(1H)-one 1223001-51-1 C24H15F3N4O 194 suppliers $65.00-$6254.00
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