Open AccessDietary cholesterol does not break your heart but kills your liver
Author(s) -
Gerhard Püschel,
Janin Henkel
Publication year - 2018
Publication title -
porto biomedical journal/porto biomedical journal
Language(s) - English
Resource type - Journals
eISSN - 2444-8672
pISSN - 2444-8664
DOI - 10.1016/j.pbj.0000000000000012
Subject(s) - hepatocyte , lipid peroxidation , steatohepatitis , fatty liver , cholesterol , oxidative stress , inflammation , steatosis , medicine , endocrinology , endoplasmic reticulum , polyunsaturated fatty acid , fibrosis , kupffer cell , lipotoxicity , chemistry , biochemistry , disease , in vitro , fatty acid , insulin resistance , insulin
Abstract It is increasingly accepted that dietary cholesterol has a much lower impact on the progression of cardiovascular disease than previously assumed. However, both animal experiments and human studies seem to support the view that dietary cholesterol may contribute to the transition from benign steatosis to the potentially fatal non-alcoholic steatohepatitis. Cholesterol esters and cholesterol accumulate in the hepatocyte and impair its function. This leads to oxidative stress and endoplasmic reticulum stress triggering the release of pro-inflammatory cytokines and rendering the hepatocyte more susceptible to apoptotic or necrotic cell death. Kupffer cells group around dying hepatocytes and phagocytose the hepatocyte debris and lipids. In addition, they are exposed to lipid peroxidation products released from hepatocytes. Kupffer cells, thus activated, release pro-inflammatory, chemotactic and profibrotic cytokines that promote inflammation and fibrosis. Therefore, dietary cholesterol may be harmful to the liver, in particular when administered in combination with polyunsaturated fatty acids that favor lipid peroxidation.