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Glutamate is also the substrate for the synthesis of GABA, which is an important paracrine signal released by the beta cell that inhibits glucagon-release from alpha cells [21, 22]

It has been hypothesized that a reduction in hepatic GCGR and signaling molecules affects a feedback mechanism acting on the pancreatic alpha cells, increasing glucagon secretion, and this liver-pancreas axis might contribute to fasting hyperglucagonemia (36)

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