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. 2021 Aug 24;12:717544. doi: 10.3389/fendo.2021.717544

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Copyright © 2021 Lu, Huang, Huang, Feng, Clark and Chen

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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GHS-R1a signaling under LEAP-2 suppression or ghrelin stimulation. G_αq – PLC – IP3 cascade on pituitary gland is responsible for GH secretion. G_αs – cAMP – PKA pathway on the NPY/AgRP neurons regulates appetite. G_αi on islet β cells inhibits cAMP – PKA signaling and subsequently prohibits GSIS. Ghrelin initiates GHS-R1a endocytosis through the activity of β-arrestin, which facilitates intracellular signaling, whereas LEAP-2 binding does not lead to receptor internalization. -, inhibit; +, activate; ↑, increase; PIP2, phosphatidylinositol 4,5-bishosphate; PLC, phospholipase C; IP3, inositol (1,4,5) triphosphate; DAG, diacylgycerol; ER, endoplasmic reticulum; [Ca²⁺], Ca²⁺ concentration; GH, growth hormone; PKC, protein kinase C; AC, adenylyl cyclase; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A; GSIS, glucose-stimulated insulin secretion; NPY/AgRP, neuropeptide Y/agouti-related protein.