Table 2.

Studies evaluating the effect of anthocyanins on hepatic lipid metabolism and hepatocellular lipotoxicity in vitro.

Paper	Anthocyanin	Food	Model	Effects	Mechanism
46	ACN-rich extract	Bilberry	Primary rat hepatocytes	⇓ tBH induced damage  ⇓ MTT, LDH, TBARS	Antioxidant
47	ACN-rich fraction	Blueberry	HepG2 cells	⇓ OA induced TG accumulation at high doses	?
48	Anthocyanin factor	Sweet potato	HepG2 cells	⇑ pAMPK  ⇓ Srepb1c, FAS	⇑ pAMPK
49	Cyanidin-3-O-β-glucoside	—	HepG2 cells	⇓ lipogenesis	⇑ pPKC ζ  ⇓ MtGPAT1 translocation to OMM
50	Cyanidin chloride	Blackberry	HepG2 cells	⇑ antioxidants (SOD, catalase)	⇑ pMAPK, ⇑ Nrf2 and PPARα
51	Cyanidin-3-O-β-glucoside	—	HepG2 cells	⇓ ROS induced by glucose ⇑ antioxidants (GSH)	⇑ PKA and CREB
52	Cyanidin-3-O-β-glucoside	—	HepG2 cells	⇑ pAMPK and pACC, ⇑ CPT1 and FFAs oxidation	AMPK activation mediated by calmodulin kinase kinase
53	ACN-rich extract	Mulberry	HepG2 cells	⇑ pAMPK and pACC, ⇑ PPARα, CPT1 and FFAs oxidation ⇓ Srebp1c and lipogenesis	AMPK activation
54	Cyanidin	—	HepG2 cells	⇓ lipogenesis ⇑ lipolysis	PPARαβ/δ agonist

AMPK: adenosine monophosphate protein kinase; Srebp1c: sterol regulated element binding protein 1c; ACC: acetyl-coenzyme A carboxylase; p: phospho; glycerol 3 phophate acyl transferase; PKC: protein kinase C; OMM: outer mitochondrial membrane; SOD: superoxide dismutase; MAPK: mitogen associated protein kinase; Nrf2: nuclear factor erythroid 2-related factor 2; PPARα: β/δ peroxisomes proliferator activated receptor α; ROS: reactive oxygen species; GSH: reduced glutathione; PKA: protein kinase A; CREB: cAMP-response element binding protein; CPT-1: carnitine-palmytoil-transferase-1; ACN: anthocyanins; OA: oleic acid; tBH: tert-butyl hydroperoxide; MTT: 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide; LDH: lactate dehydrogenase; TBARS: thiobarbituric acid reacting substances.