Visceral fat: A key mediator of steatohepatitis in metabolic liver disease

By D. K. van der Poorten, Kerry‐Lee Milner, J. Hui, A. Hodge, M. Trenell, J. Kench, R. London, Tony Peduto, D. Chisholm, J. George. Hepatology, 2008

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Pathogenesis of non-alcoholic fatty liver disease (2009, background): “Similarly, serum IL-6 levels are also elevated in both animal and human models of IR and NAFLD,(43,50,51) and levels correlate with increasing liver inflammation and fibrosis.(52) The key role of hepatocyte cytokine production in the progression of steatosis to NASH is supported by studies demonstra”
Treatment of NAFLD with diet, physical activity and exercise. (2017, background): “The precise mechanism of how visceral fat applies its detrimental effects on liver metabolism, fibrotic and inflammatory consequences remain unclear, although influx of fatty acids and synthesis of cytokines and adipokines has been shown to promote liver lipid accumulation, insulin resistance and in”
Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Hepatic inflammation and fibrosis correlate with the amount of visceral fat.(75) Trunk fat has been shown to be a major factor leading to increased serum alanine aminotransferase levels, which might reflect more advanced disease such as NASH.”
Cafeteria Diet Is a Robust Model of Human Metabolic Syndrome With Liver and Adipose Inflammation: Comparison to High-Fat Diet (2011, background): “Hepatosteatosis and steatohepatitis lead to liver insulin insensitivity and the inability to blunt gluconeogenesis, which is another contributing factor to metabolic syndrome (39).”