Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis.

By C. Koliaki, J. Szendroedi, K. Kaul, T. Jelenik, P. Nowotny, Frank Jankowiak, C. Herder, M. Carstensen, M. Krausch, W. Knoefel and 2 more. Cell Metabolism, 2015

919 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/b7fcd9666f33a60be9e99ee563ad8d614671b2e8

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In Epidemiology

1. P. Tveden‐Nyborg
2. S. Tait
3. Joel S. Riley
4. D. H. Ipsen
5. J. Lykkesfeldt

Citations in the corpus

• Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “291 Recent research also highlighted the role of autophagy-related gene 3 (ATG3) in steatosis during NAFLD progression, with studies indicating that knock-down of hepatic ATG3 could improve fatty acid metabolism and enhance mitochondrial complex activity, partly by reducing c-Jun N-terminal protein…”
• Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease (2018, background): “Decreased activity of the mitochondrial respiratory chain was reported in overweight/obese patients with NASH compared to controls [97, 98], and alterations in mitochondrial ultrastructure have been observed prior to NAFLD development in the Otsuka Long–Evans Tokushima Fatty rat [99] as well as in p”
• Mitochondrial DNA in inflammation and immunity (2020, positive): “The precise ligand for TLR9-derived liver disease was poorly understood, although the observation that NASH patients had higher mitochondrial mass, but reduced respiration, suggested that mitochondria may play a role [182].”