. Author manuscript; available in PMC: 2020 Feb 4.

Published in final edited form as: Clin Gastroenterol Hepatol. 2018 Oct 4;17(2):322–332. doi: 10.1016/j.cgh.2018.10.002

Table 1.

Selected Sample of Gut Microbiota to Brain Signaling Channels

Input	Output	Study

2BAs	Improved central regulation of glucose metabolism via production of FGF19	Marcelin et al⁸
		Ryan et al⁹
	Suppression of HPA axis via production of FGF19	Perry et al¹⁰
	GLP-1 and PYY release from L cells via TGR5 receptor	Bala et al¹¹
	Synthesis and release of 5-HT from ECCs	Yano et al³
SCFAs	PYY, GLP-1, and GLP-2 release from L cells	Cani et al¹²
	Leptin production from adipocytes via GPR41	Xiong et al¹³
	Synthesis and release of 5-HT from ECCs	Yano et al³
Indole	GLP-1 secretion from L cells via interaction with voltage-gated potassium channels and mitochondrial NADH dehydrogenase	Chimerel et al¹⁴
	Kynurenine synthesis via activation of AhR	Vogel et al¹⁵
TLR ligands: LPS, flagellin, and so forth	CCK synthesis from EECs via TLRs	Palazzo et al¹⁶
	PYY expression in vitro from L cells via TLRs	Larraufie et al¹⁷
	5-HT release in vitro from ECCs via TLRs	Kidd et al¹⁸

NOTE. The table outlines well-characterized signaling channels driving bottom-up communication along the brain gut microbiota axis. Each input represents a microbiota-derived intermediate that results in a physiological output by interacting with host cells or host-derived signaling molecules.

5-HT, serotonin; CCK, cholecystokinin; ECC, enterochromaffin cell; EEC, enteroendocrine cell; FGF19, fibroblast growth factor 19; GLP, glucagon-like peptide; HPA, hypothalamic pituitary adrenal; LPS, lipopolysaccharide; NADH, nicotinamide adenine dinucleotide; PYY, peptide YY; TGR5, Takeda G-protein-coupled receptor 5; TLR, Toll-like receptor