Human Fatty Liver Disease: Old Questions and New Insights
By Jonathan C. Cohen, Jay D. Horton, Helen H. Hobbs. Science, 2011
2,072 citations recorded by the source corpus.
Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem that affects one-third of adults and an increasing number of children in developed countries. The disease begins with the aberrant accumulation of triglyceride in the liver, which in some individuals elicits an inflammatory response that can progress to cirrhosis and liver cancer. Although NAFLD is strongly associated with obesity and insulin resistance, its pathogenesis remains poorly understood, and therapeutic options are limited. Here, we discuss recent mechanistic insights into NAFLD, focusing primarily on those that have emerged from human genetic and metabolic studies.
Subfields: Biochemistry, Endocrinology, Diabetes and Metabolism, Epidemiology
View Paper: https://www.semanticscholar.org/paper/4cbfbb2a3f311acf9bce734925b6f17d7b99d12b
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In Biochemistry
In Endocrinology, Diabetes and Metabolism
In Epidemiology
- Tiangang Li
- Gerald I. Shulman
- P. Scherer
- J. Y. Chiang
- Y. Kawano
- D. Cohen
- Laura E. Nagy
- Andreas L. Birkenfeld
Citations in the corpus
- Palmitic Acid: Physiological Role, Metabolism and Nutritional Implications (2017, background): “…that desaturation of de novo synthesized FA may be required to modulate TAG biosynthesis and prevent lipotoxic effects by excessive saturated fat accumulation (Collins et al., 2010), and consequent cellular dysfunction involved in the metabolic syndrome (Brookheart et al., 2009; Cnop et al., 2012).”
- Bile Acid Metabolism and Signaling (2013, neutral): “OCA has been in phase II clinical trials type 2 diabetic patients with NAFLD.”
- Bile Acid Signaling in Metabolic Disease and Drug Therapy (2014, background): “The therapeutic potential of bile acids and derivatives for treating hepatic and biliary diseases, NAFLD, and metabolic syndrome has been extensively reviewed (Thomas et al., 2008; Fiorucci and Baldelli, 2009; Zollner and Trauner, 2009; Lian et al., 2011; Pols et al., 2011a,b; Adorini et al., 2012; ”
- Adiponectin, Leptin, and Fatty Acids in the Maintenance of Metabolic Homeostasis Through Adipose Tissue Crosstalk (2016, background): “NAFLD and NASH can be associated with insulin resistance, though not in all cases, and a subgroup of individuals among this group has a higher risk of progressing to cirrhosis and, eventually, hepatocellular carcinoma (Cohen et al., 2011; Starley et al., 2010).”
- FAT SIGNALS - Lipases and Lipolysis in Lipid Metabolism and Signaling (2012, background): “A role for neutral lipid metabolism in signaling gained substantial interest when it was noted that increased cellular TG concentrations are strongly associated with insulin resistance in skeletal muscle and liver (Cohen et al., 2011; Kelley et al., 2002).”
- Mechanisms of Hepatic Triglyceride Accumulation in Nonalcoholic Fatty Liver Disease (2013, positive): “In the setting of excess carbohydrates, fatty acids are also synthesized de novo within the liver [1].”
- Non Alcoholic Fatty Liver Disease, Hepatic Insulin Resistance and Type 2 Diabetes (2014, background): “N onalcoholic fatty liver disease (NAFLD) affects up to 30% of adults and up to 10% of children in developed countries.(1,2) The disease begins with the accumulation of triacylglycerol (TAG) in the liver and is defined as the presence of cytoplasmic lipid droplets in more than 5% of hepatocytes or T”
- Kupffer Cells in the Liver (2013, positive): “Similar to the rates of progression of ALD, not all obese individuals develop metabolic syndrome and NAFLD/NASH, suggesting a role for environmental and/or genetic contributions to the progression of liver injury (20).”