Fig. 5: MCJ silencing enhances β-oxidation and prevents lipid accumulation in hepatocytes in vitro and in vivo.

a–j Mice were placed on mMCD diet 1 week prior to the initiation of the treatment and maintained on the diet for the duration of the study. Treatment with Invivofectamine-formulated siMCJ (n = 5) or siRNAc (n = 5) was given weekly for 3 weeks. Tissues were harvested 1 week after the last dose. a Oxygen consumption rate (OCR) using the Seahorse analyzer. b ATP levels in isolated mitochondria. c Rate of fatty acid oxidation determined by the production of acid soluble metabolites (ASM). d Rate of fatty acid oxidation determined by the production of CO₂. e mRNA expression of fatty acid oxidation genes in siMCJ-treated liver relative to control liver, as determined by real time RT-PCR. f De novo lipogenesis of fatty acids (FA), diglycerides (DG), and triglycerides (TG) in the liver. g Triglycerides levels and (h) ketone bodies levels in serum. i Activity of malate dehydrogenase (MDH2) in liver extracts. j Glutathione (GSH) levels in liver. k-l Primary hepatocytes from WT mice were transfected with siRNAc or siMCJ and were incubated with steatosis-inducing doses of oleic acid alone for 24 h or in combination with rotenone for the last 6 h. k Representative images of lipid content and (l) quantification evaluated by Bodipy staining. *denotes p < 0.05, as determined by Student’s t test analysis. Error bars show standard error (SE) in all the panels except panels (e) and (f) where error bars show standard deviation (SD). Source data are provided as a Source Data file.