Mitochondrial abnormalities in non-alcoholic steatohepatitis

Background/Aims: We assessed mitochondrial morphology by electron microscopy and the prevalence of a mitochondrial gene deletion in patients with nonalcoholic steatohepatitis (NASH), alcohol-related liver disease and non-fatty liver diseases. Respiratory chain function using a cytoplasmic hybrid (cybrid) assay was further studied in NASH patients and healthy controls, Methods: Electron microscopy was performed in 26 specimens. Fifteen patients were studied by polymerase chain reaction to detect a 520-bp deletion product of the mitochondrial genome (dmtDNA). Cybrids were created by fusion of platelets with anaerobic neuroblastoma cells in sis NASH patients and 12 controls, Results: Eight of ten NASH, one of seven alcoholics and two of nine other patients had linear crystalline inclusions in megamitochondria (p<0.05). Three of five patients with alcohol-related li cer disease had dmtDNA compared to one of live NASH patients and one of five non-steatohepatitis controls, Cybrid respiratory chain function in platelets was not different from that of controls, Conclusions: Respiratory chain dysfunction, if present in NASH, is not expressed in platelet-derived mitochondria. In contrast to alcohol-related liver disease with active drinking, NASH patients do not commonly express the 5-kb mitochondrial DIVA gene deletion in liver tissue, As previously described in early alcohol-related liver disease, crystalline inclusions of unknown composition are seen in hepatic mitochondria in NASH, Their presence suggests either an adaptive process or mitochondrial injury.