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Table 1 Drugs or compounds identified to have therapeutic effects on NAFLD and their mechanisms related to MAMs

From: Mutual interaction between endoplasmic reticulum and mitochondria in nonalcoholic fatty liver disease

Drug or compoundAnimalsMechanism(s)Reference(s)
Rosiglitazoneob/ob and diet-induced insulin-resistant mice, CypD-KO miceIncreased MAM numbers in primary hepatocytes with overexpression of CypD, VDAC1 and PACS2, enhanced insulin signalling and action.[94]
Metforminob/ob and diet-induced insulin-resistant mice, CypD-KO miceImproved ER-mitochondria interactions.[94, 125]
ForskolinHuH7 cells treated with glucosePrevention of high glucose-mediated reductions in MAM integrity[89]
Sulforaphaneob/ob mice and HFHSD mice, primary mouse hepatocytes treated with palmitate in vitroImproved glucose tolerance, MAM protein content and ER–mitochondria interactions; decreased levels of the ERS markers CHOP and Grp78[125, 126]
Hepatic stimulator substance (HSS)Mice fed a methionine and choline-deficient dietImproved expression of SERCA, maintenance of Ca2+ homeostasis within MAMs[127]
TroglitazoneSprague–Dawley ratsReduced ACS activity in the liver MAM component and the peroxisome component[128, 129]