Table 2.

Summary of metabolomic studies examining the development of NASH

species [ref]	tissue	platform	up-regulated	down-regulated	conclusions
Human [9 obese with normal liver; 24 NAFLD; 9 NASH] [10]	serum	UPLC- ESI- QTOFMS	NASH vs. NAFLD: PC(14:0/20:4), LPC(18:1)	NASH vs. NAFLD: LPC(24:0)	A few lipid changes between NAFLD and NASH of uncertain origin.
Human 28 HV; 6 NASH	serum	NMR	Glucose, glutamate, taurine	-	Increased glucose mobilization.
Humans [HV 50; NASH 50] [7]	plasma	HPTLC GCFID LCMS	Triacylglycerols, FAs: 14:1n5, 16:1n7, 18:1n9, 18:1n7, 18:3n6, 20:3n6, 22:6n3, 5-HETE, 8-HETE, 15-HETE, 11-HETE		lipogenesis↑
Human [25 HV; 24 NASH] [9]	plasma	UPLC- ESI- TQMS GCMS	N-Acetylthreonine, aspartate, glutamate, phenylalanine, tyrosine, 3-(4-hydroxyphenyl)-lactate, kynurenine, isoleucine, leucine, valine, ornithine, glutamylvaline, γ-glutamyl-leucine, γ-glutamyl-phenylalanine, γ-glutamyl-tyrosine, erythronate, mannose, glucose, pyruvate, lactate,2-oxoglutarate, carnitine, propionylcarnitine, butyrylcarnitine, 2-methybutyroylcarnitine, GCA, TCA, GCDCA, xanthine, urate, pseudouridine, erithritol	N-Acetylglycine, betaine, histidine, phenylacetate, indolepropionate, 2-aminobutyrate, cysteine-glutathione disulfide, glycerate, 20:5n3, 22:6n3, 11:1n1, 20:4n6, 2-hydroxypalmitate, 3-carboxy-4-methyl-5-propyl-2-furanpropanoate, glycerophosphocholine, LPC(18:1), LPC(18:2), LPC(20:4), cortisone, threonate, hippurate, catechol sulfate, indoleacrylate, 3-phenylpropionate	Elevated bile acids GCA, TCA and GCDCA a sign of liver injury or insulin resistance. High rate of GSH turnover reflective of oxidative stress. Origin of certain depressed PUFAs and LPCs uncertain. Increased glucose mobilization and formation of pyruvate and lactate suggests cytosolic glycolysis. Elevation of essential amino acids suggests increased protein turnover.
Mouse fed methionine- and choline-deficient diet [11]	serum	UPLC- ESI- QTOFMS	Tauro-β-muricholate, TCA, 12-HETE	LPC(16:0), LPC(18:0), LPC(18:1)	Disruption of bile acid and phospholipid homeostasis due to hepatic inflammatory signaling.

For abbreviations, see Table 1 footnotes.