Molecular mediators of hepatic steatosis and liver injury.

By J. Browning, Jay D. Horton. Journal of Clinical Investigation, 2004

2,066 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/075156cc7c5280c5a39bc9fa6e8ec5fcab1bd9be

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology, Diabetes and Metabolism

1. Gerald I. Shulman
2. V. Samuel
3. S. Friedman
4. Q. Anstee
5. Robert D. Goldin
6. Martin Adiels
7. S. Olofsson
8. R. Loomba

In Epidemiology

1. Gerald I. Shulman
2. V. Samuel
3. Q. Anstee
4. S. Friedman
5. Robert D. Goldin
6. A. Sanyal
7. R. Loomba
8. L. Guidotti

In Surgery

1. Jonathan C. Cohen
2. Martin Adiels
3. S. Olofsson
4. Helen H. Hobbs
5. Marja-Riitta Taskinen
6. Gerald I. Shulman
7. S. Friedman
8. L. Guidotti

Citations in the corpus

• Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease (2008, background): “The accumulation of excess triglyceride in the liver, a condition known as hepatic steatosis (or fatty liver), is associated with adverse metabolic consequences, including insulin resistance and dyslipidemi”
• Fibroblast Growth Factor 21 Reverses Hepatic Steatosis, Increases Energy Expenditure, and Improves Insulin Sensitivity in Diet-Induced Obese Mice (2009, background): “SREBP-1 is a transcription factor critical for lipogenesis and is involved in the induction of hepatic steatosis in several animal models (29,30).”
• AMPK Phosphorylates and Inhibits SREBP Activity to Attenuate Hepatic Steatosis and Atherosclerosis in Diet-induced Insulin Resistant Mice (2011, neutral): “The dysregulation of SREBP-1c has been implicated in the pathogenesis of hepatic steatosis, dyslipidemia, and type 2 diabetes (Raghow et al., 2008; Browning and Horton, 2004).”
• Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. (2019, background): “Although the mechanism(s) responsible for the increase in hepatic DNL in people with NAFLD is not known, it is possible that increases in circulating insulin and glucose associated with hepatic and whole-body insulin resistance are involved in stimulating hepatic DNL because insulin and glucose acti”
• Excessive Hepatic Mitochondrial TCA Cycle and Gluconeogenesis in Humans with Nonalcoholic Fatty Liver Disease (2011, background): “Nonalcoholic fatty liver disease (NAFLD) is associated with obesity and insulin resistance and affects approximately onethird of the U.S. population (Browning and Horton, 2004; Browning et al., 2004; Clark et al., 2002).”
• Hepatocyte-specific Deletion of SIRT1 Alters Fatty Acid Metabolism and Results in Hepatic Steatosis and Inflammation (2009, background): “Dysregulation of lipid metabolic pathways results in the development of hepatic steatosis and contributes to the development of chronic hepatic inflammation, insulin resistance, and liver damage (Browning and Horton, 2004; Samuel et al., 2004; Sanyal, 2005).”
• Histopathology of pediatric nonalcoholic fatty liver disease (2005, background): “3) Laboratories, mean (SD) AST (U/L) 65 (43) 52 (30) 79 (52) 79 (34) 65 (47) ALT (U/L) 104 (91) 69 (35) 131 (115) 119 (58) 106 (104) GGT (U/L) 58 (38) 37 (17) 61 (36) 59 (33) 66 (44) Triglyceride (mg/dL) 181 (88) 161 (104) 192 (63) 195 (98) 174 (89) QUICKI 0.”
• Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, neutral): “tional regulator of de novo lipogenesis (17).”