Nonalcoholic steatohepatitis: association of insulin resistance and mitochondrial abnormalities.

By A. Sanyal, Carol Campbell-Sargent, F. Mirshahi, W. Rizzo, M. Contos, R. Sterling, V. Luketic, M. Shiffman, J. Clore. Gastroenterology, 2001

2,135 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/278919dd21687e900e1bbd17755e49155716be30

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Citations in the corpus

Non-Alcoholic Fatty Liver Disease (NAFLD) and Its Connection with Insulin Resistance, Dyslipidemia, Atherosclerosis and Coronary Heart Disease (2013, positive): “Several studies have highlighted that insulin resistance is a characteristic feature of NAFLD [10–12], even when subjects are not obese [13].”
Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “One of the final common mediators of IR seems to be oxidative stress due to generation of reactive oxygen species (ROS) and/or decreased antioxidant defenses (108).”
Nonalcoholic fatty liver disease: a feature of the metabolic syndrome. (2001, background): “In all patients, using metformin or glitazones to increase hepatic sensitivity to insulin might break the vicious circle linking hyperinsulinemia and insulin resistance to elevated triglyceride and FFA concentrations, progressive steatosis, ultrastructural mitochondrial lesions in the hepatocytes, a”
Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. (2015, positive): “As a result, the ratio of ETC complex expression to CSA was even lower in NASH, indicating lower density of functional mitochondria, in line with reports of abnormal mitochondrial morphology in livers of NASH patients (Sanyal et al., 2001).”
Excessive Hepatic Mitochondrial TCA Cycle and Gluconeogenesis in Humans with Nonalcoholic Fatty Liver Disease (2011, background): “Indeed, individuals with NASH have elevated circulating ketones (Sanyal et al., 2001), and obese humans have a 2-fold increase in hepatic (11)C-palmitate oxidation by positron emission tomography (Iozzo et al.”
The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “[35] Sanyal AJ, Campbell-Sargent C, Mirshahi F, et al.”
Adiponectin, a Therapeutic Target for Obesity, Diabetes, and Endothelial Dysfunction (2017, background): “This attenuation in the activity of the respiratory chain would results from an accumulation of reactive oxygen species (ROS) that oxidize stored fats to form lipid peroxidation products, which ultimately leads to steatohepatitis, necrosis, inflammation, and fibrosis [103].”
The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “Hepatocytic lipid accumulation predisposes to overproduction of reactive oxygen species (ROS), endoplasmatic reticulum (ER) stress and lipotoxicity [6–8].”
A lipidomic analysis of nonalcoholic fatty liver disease (2007, methodology): “(TAG), free cholesterol (FC), cholesterol esters (CEs), and PLs in normal livers and compare them to those of NAFL and NASH and (2) compare the distribution of fatty acids within each of these classes in these groups of subjects.”
Nonalcoholic fatty liver disease: pathology and pathogenesis. (2010, background): “Oxidative stress (defined as an imbalance in the production of ROS and protective antioxidants) has often been linked to NAFLD (86, 87), and may be a final common mechanistic occurrence in the lipotoxicity of FFA (57, 56).”