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In humans, excess cholesterol in the blood is captured by low-density lipoprotein (LDL) and removed by the liver via endocytosis of the LDL receptor. [4] Recent evidence indicates that the members of the LDL receptor gene family are active in the cell signalling pathways between specialized cells in many, if not all, multicellular organisms. [5 ...
When LDL receptors bind LDL particles in the bloodstream, the clathrin-coated pits are endocytosed into the cell. [citation needed] Vesicles containing LDL receptors bound to LDL are delivered to the endosome. In the presence of low pH, such as that found in the endosome, LDL receptors undergo a conformation change, releasing LDL. LDL is then ...
After internalization, the receptors dissociate from their ligands when they are exposed to lower pH in endosomes. After dissociation, the receptor folds back on itself to obtain a closed conformation and recycles to the cell surface. [22] The rapid recycling of LDL receptors provides an efficient mechanism for delivery of cholesterol to cells.
Fibrates may decrease LDL, though generally to a lesser degree than statins. Similar to statins, the risk of muscle damage exists. Nicotinic acid, like fibrates, is also well suited for lowering triglycerides by 20–50%. It may also lower LDL by 5–25% and increase HDL by 15–35%. Niacin may cause hyperglycemia and may also cause liver damage.
interference with the heart's blood supply, typically by clogging of coronary, or other, arteries. Ischemia means lack of oxygen which necessarily follows from one or more blocked arteries. Coxsackie B4 virus a virus which can trigger an auto-immune reaction which eventually results in a (mistaken) auto-immune attack on the beta cells.
Obesity has been found to contribute to approximately 55% of cases of type 2 diabetes; [10] chronic obesity leads to increased insulin resistance that can develop into type 2 diabetes, [11] most likely because adipose tissue (especially that in the abdomen around internal organs) is a source of several chemical signals, hormones and cytokines, to other tissues.
Oxidized low-density lipoprotein receptor 1 (Ox-LDL receptor 1) also known as lectin-type oxidized LDL receptor 1 (LOX-1) is a protein that in humans is encoded by the OLR1 gene. [ 5 ] [ 6 ] LOX-1 is the main receptor for oxidized LDL on endothelial cells , macrophages , smooth muscle cells , [ 7 ] and other cell types. [ 8 ]
The uptake of LDL-C alone does not cause foam cell formation; however, the co-internalization of LDL-C with modified LDL in macrophages can result in foam cell development. Modified LDL affects the intracellular trafficking and metabolism of native LDL, such that not all LDL need to be modified for foam cell formation when LDL levels are high.