Abstract
Previous studies have revealed that a high-fat diet is one of the key contributors to the progression of liver fibrosis, and increasing studies are devoted to analyzing the different influences of diverse fat sources on the progression of non-alcoholic steatohepatitis. When we treated three types of isocaloric diets that are rich in cholesterol, saturated fatty acid (SFA) and trans fatty acid (TFA) with hepatitis C virus core gene transgenic mice that spontaneously developed hepatic steatosis without apparent fibrosis, TFA and cholesterol-rich diet, but not SFA-rich diet, displayed distinct hepatic fibrosis. This review summarizes the recent advances in animal and cell studies regarding the effects of these three types of fat on liver fibrogenesis.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a disease entity that includes nonalcoholic fatty liver (NAFL, presence of hepatic steatosis without other liver damage) and non-alcoholic steatohepatitis (NASH, infiltration of inflammatory cells, presence of hepatocellular degeneration with and without irreversible fibrosis), and NAFLD may progress into liver cirrhosis and cancer [1,2,3,4,5]
Wobser et al revealed that the conditioned media (CM) of steatotic hepatocytes incubated with palmitate initiated the activation of hepatic stellate cells (HSC), as evidenced by the increased production of α-smooth muscle actin (α-SMA) and type 1 collagen [87]
This review summarized possible mechanisms of three different lipids on parenchymal and non-parenchymal liver cells, which differentially contributed to the development of steatohepatitis and steatofibrosis
Summary
Non-alcoholic fatty liver disease (NAFLD) is a disease entity that includes nonalcoholic fatty liver (NAFL, presence of hepatic steatosis without other liver damage) and non-alcoholic steatohepatitis (NASH, infiltration of inflammatory cells, presence of hepatocellular degeneration with and without irreversible fibrosis), and NAFLD may progress into liver cirrhosis and cancer [1,2,3,4,5]. 2021, 22, 10303 animal and cell studies would provide clue to clarify the impact of specific dietary fat on the progression of liver disease [13]. To uncover the influence of a diet enriched in cholesterol, saturated fatty acids (SFA), and trans fatty acids (TFA) onofhepatic steatosisinand ensuing liver disorders, hepatitis. To uncover the influence a diet enriched cholesterol, saturated fatty acids (SFA), and (TFA)(HCVcpTg) on hepatic mice steatosis ensuing liver disorders, hepatitis virustrans core fatty gene acids transgenic that and spontaneously developed hepatic steatovirus core gene transgenic (HCVcpTg) mice that spontaneously developed hepatic steatosis sis without apparent fibrosis were used [14,15,16,17]. We have investigated the impact of dietary lipids, especially cholesterol, SFA, and in this review, we focused on these three lipids and summarized their influence on TFA. We focused on these three lipids and summarized their influence fibrosis and on liver fibrosis and the possible mechanisms
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