Defective hepatic mitochondrial respiratory chain in patients with nonalcoholic steatohepatitis

By M. Pérez-Carreras, P. del Hoyo, Miguel Ángel Martín, J. Rubio, Ana Martín, G. Castellano, F. Colina, J. Arenas, J. Solís-Herruzo. Hepatology, 2003

716 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/ff72d7bba67f064da8a166bebfda4c39d248113b

How researchers see this paper

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In Endocrinology, Diabetes and Metabolism

1. A. Sanyal
2. Gerald I. Shulman
3. V. Samuel

In Epidemiology

1. A. Sanyal
2. P. Newsome
3. J. Browning
4. J. Tomlinson
5. J. Dowman
6. Gerald I. Shulman
7. V. Samuel

In Physiology

1. Gerald I. Shulman
2. V. Samuel

Citations in the corpus

• Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. (2015, neutral): “, 2002) and adjusted to individual CSA values to account for mitochondrial content, in line with the majority of studies in this field (Mantena et al., 2009; Pérez-Carreras et al., 2003; Satapati et al., 2012) (for methods see Supplemental Experimental Procedures).”
• Excessive Hepatic Mitochondrial TCA Cycle and Gluconeogenesis in Humans with Nonalcoholic Fatty Liver Disease (2011, background): “In fact, defects in hepatic mitochondria or the function of oxidative phosphorylation similar to skeletal muscle are typically observed only during NASH or diabetes (Caldwell et al., 2009; Cortez-Pinto et al., 1999; Pérez-Carreras et al., 2003; Szendroedi et al., 2009).”
• INCREASED HEPATIC SYNTHESIS AND DYSREGULATION OF CHOLESTEROL METABOLISM IS ASSOCIATED WITH THE SEVERITY OF NONALCOHOLIC FATTY LIVER DISEASE (2012, background): “NASH is also associated with a decrease in CYP7A and CYP27A levels; CYP27A is a mitochondrial protein and its decrease may reflect mitochondrial injury that is present in NASH but not in NAFL (Caldwell et al., 2009; Pérez-Carreras et al., 2003).”
• Molecular mediators of hepatic steatosis and liver injury. (2004, neutral): “The ultrastructural mitochondrial defects in patients with NAFLD may be indicative of defective oxidative-phosphorylation, inas-much as these patients also have reduced MRC activity (73) and impaired ATP synthesis after a fructose challenge (74).”
• Pathogenesis of non-alcoholic fatty liver disease (2009, background): “Structural mitochondrial abnormalities 71 and a reduction in mitochondrial respiratory chain activity have been observed in human studies of NASH.”