Amino Acid Transporter Slc38a5 Controls Glucagon Receptor Inhibition-Induced Pancreatic α Cell Hyperplasia in Mice

Glucagon supports glucose homeostasis by stimulating hepatic gluconeogenesis, in part by promoting the uptake and conversion of amino acids into gluconeogenic precursors. Genetic disruption or pharmacologic inhibition of glucagon signaling results in elevated plasma amino acids and compensatory gluc...

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Bibliographic Details
Published in:	Cell metabolism Vol. 25; no. 6; pp. 1348 - 1361.e8
Main Authors:	Kim, Jinrang, Okamoto, Haruka, Huang, ZhiJiang, Anguiano, Guillermo, Chen, Shiuhwei, Liu, Qing, Cavino, Katie, Xin, Yurong, Na, Erqian, Hamid, Rachid, Lee, Joseph, Zambrowicz, Brian, Unger, Roger, Murphy, Andrew J., Xu, Yan, Yancopoulos, George D., Li, Wen-hong, Gromada, Jesper
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 06-06-2017
Subjects:	Amino Acid Transport Systems, Neutral - genetics Amino Acid Transport Systems, Neutral - metabolism amino acid transporter Animals glucagon Glucagon - genetics Glucagon - metabolism glucagon receptor glucagon receptor knockout Glucagon-Secreting Cells - metabolism Glucagon-Secreting Cells - pathology hyperaminoacidemia Hyperplasia Male Mice Mice, Inbred ICR Mice, Knockout mTORC1 pancreatic alpha cell proliferation Receptors, Glucagon - genetics Receptors, Glucagon - metabolism Signal Transduction Slc38a5 pancreatic alpha cell hyperaminoacidemia proliferation glucagon receptor Slc38a5 glucagon receptor knockout glucagon mTORC1 amino acid transporter
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