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. Author manuscript; available in PMC: 2018 Jun 6.
Published in final edited form as: Cell Metab. 2017 Jun 6;25(6):1362–1373.e5. doi: 10.1016/j.cmet.2017.05.011

Figure 6. Model for liver-pancreatic islet α-cell axis where L-glutamine and glucagon reciprocally regulate each other.

Figure 6

Glucagon is released from pancreatic islet α-cells where it acts on hepatocyte GCGRs to stimulate gluconeogenesis and hepatic glucose output, raising blood glucose. Interrupted glucagon signaling in hepatocytes leads to decreased AA catabolism and increased circulating AA. Of these AA, Q selectively activates α-cell proliferation through both FoxP- and mTOR-dependent mechanisms. mTOR activation in the α-cell leads to upregulation of Slc38a5 expression that further potentiates Q-dependent α-cell proliferation completing an endocrine feedback loop between liver and pancreatic islet α-cells. Glutaminase 2-GLS2, mechanistic target of rapamycin-mTOR, amino acids-AAs.