Interpreting lipoproteins in nonalcoholic fatty liver disease

Abstract

Physicians should infer from biomarkers or clinical findings that their abdominally obese patients are at risk of severe cardiovascular, liver fatty disease, or both. Physicians should carry out laboratory tests of plasma cholesterol, triglycerides, LDL and HDL cholesterol, non-HDL cholesterol, apolipoprotein B and platelets, and for diabetes, but importantly, plasma triglycerides also in the nonfasting state. But note, clinical routine plasma lipid and lipoprotein measurements are not necessarily reliable for interpreting severe metabolic changes. Notably, in advanced stages of NAFLD (i.e., late steatohepatitis and cirrhosis), routine lipid profiles do not necessarily show any more abnormalities.

Interaction between alcohol consumption and metabolic syndrome in predicting severe liver disease in the general population

“…NAFLD is associated with a lipid profile characterized by a high serum triglyceride level, low HDL cholesterol level, high triglyceride‐rich very low‐density lipoprotein (VLDL) level, and accumulation of small‐dense LDL . VLDL is associated with NAFLD severity …”

“…NAFLD is associated with a lipid profile characterized by a high serum triglyceride level, low HDL cholesterol level, high triglyceride-rich very low-density lipoprotein (VLDL) level, and accumulation of smalldense LDL. (33) VLDL is associated with NAFLD severity. (34) It could be speculated that a high total-to-LDL cholesterol ratio reflects a state where a larger proportion than normal of plasma cholesterol is in the form of non-LDL lipoproteins such as VLDL (reflected by total cholesterol) and a reduced proportion in LDL.…”

Mutual interaction between endoplasmic reticulum and mitochondria in nonalcoholic fatty liver disease

“…Cholesterol is exchanged and transported through cholesterol ester transfer protein (CETP), while the remaining phospholipids, ApoE and ApoC, in VLDL are transferred to high-density lipoprotein (HDL), and VLDL is transformed into VLDL residues. Most of these residues are then integrated into the liver through the VLDL receptor, while a few are converted into low-density lipoprotein (LDL) to continue metabolism [27]. A total of 65-70% of LDL in plasma is cleared by LDL receptors, and a small proportion (approximately 1/3) is taken up by the surrounding tissues (including the liver) and dissimilated.…”

“…A total of 65-70% of LDL in plasma is cleared by LDL receptors, and a small proportion (approximately 1/3) is taken up by the surrounding tissues (including the liver) and dissimilated. Most VLDL residues are converted to LDL and recognized by liver LDL receptors under normal conditions; thus, LDL receptor dysfunction leads to increases in plasma LDL concentrations [26,27].…”

Vésicules extracellulaires, biomarqueurs et bioeffecteurs du syndrome métabolique

“…Elle peut également fusionner, après endocytose, avec les endosomes dans le cytoplasme. [17]. L'accumulation de LDL dans les monocytes-macrophages infiltrés dans la paroi vasculaire facilite leur transformation en cellules spumeuses menant à la formation de la plaque d'athérome.…”