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Background  Nonalcoholic fatty liver disease is a common disorder that progresses from simple fatty liver (steatosis) to nonalcoholic steatohepatitis (NASH). It is thought that mitochondrial dysfunction plays a critical role in the progression of NASH. In this study, we developed a non-invasive method for early diagnosis and staging of NASH that directly measures mitochondrial complex-I (MC-I) activity in the liver of NASH model mice by positron emission tomography (PET) imaging using the novel tracer 2-tert-butyl-4-chloro-5-[6-(4-[ 18 F]fluorobutoxy)-pyridin-3-ylmethoxy]-2H-pyridazin-3-one ( 18 F-BCPP-BF). Liver uptake of  18 F-BCPP-BF in NASH and age-matched control mice was measured as a standard uptake value over a period of 1 to 12 weeks. Histopathological evaluation of the liver tissue was performed by haematoxylin and eosin staining, and fibrosis was assessed by Masson’s trichrome staining.    Results  Significant mitochondrial dysfunction was detected as early as 1 week after commencing the diet, and MC-I activity in the liver measured by PET was reduced by &gt; 50% relative to that in age-matched control mice after 6 weeks. Liver uptake of  18 F-BCPP-BF was low throughout the 12-week experimental period. Histopathological examination revealed that steatosis, inflammation, and ballooning progressed from 1 to 6 weeks, with fibrosis observed from 6 to 12 weeks.    Conclusions  PET scans and histopathological analysis revealed that mitochondrial dysfunction in the liver contributed to the progression of NASH. PET imaging with  18 F-BCPP-BF is a useful tool for detecting NASH at early stages and for monitoring therapeutic response.

Sensitive and early detection of mitochondrial dysfunction in the liver of NASH model mice by PET imaging with 18F-BCPP-BF