Triglycerides receptor sakar6 VLDL biogenesis as an endogenous source

Triglycerides composed of one glycerol molecule attached to three fatty acids. Dietary as an exogenous source of TG are hydrolyzed in the stomach and small intestine to form fatty acids and 2-monoacylglycerol to absorb by Enterocytes Sakar1 After a meal, chylomicrons that are triglyceride-rich lipoproteins (TRL) produce and export from enterocytes into lymph before transporting to the circulation Sakar2 subsequently, chylomicrons hydrolyzes by Lipoprotein lipase (LPL) into fatty acids that provide energy to the heart and skeletal muscles or stored in adipose tissue. sakar(3. 4)  Chylomicron remnants are removed from the circulation after binding to the LDL receptor sakar6


VLDL biogenesis as an endogenous source of triglyceride occurs by hepatocytes and delivered to ?peripheral tissues, where they are used as energy by heart and muscle or stored in adipose tissue ?as a long-term TG reservoir when more calories are consumed than the body requires  sakar3  However, the excess TG after a meal rich in dietary fat temporary store in cytoplasmic lipid droplet (CLDs) to prevent lipotoxicity sakar10

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Hypertriglyceridemia may contribute to atherosclerosis, CVD, diabetes mellitus, pancreatitis, ?body mass index, inflammation, metabolic syndrome, for management TG in a borderline ?screening and observation fasting TG and post-prandial (non-fasting) are recommended, however ?fasting TG levels are more reliable than post-prandial TG levels ? sakar11


Nonetheless, the main causes of Hypertriglyceridemia are fat and carbohydrate-rich diet, obesity, waist circumference, ?alcohol, stress, and lifestyle but many studies suggesting that genetic polymorphisms may underlie ?Hypertriglyceridemia. sakar11 Many genes that involved in the triglyceride biosynthetic pathway (stearoyl-CoA desaturases, fatty ?acid synthesis, diglyceride acyltransferase-2), overproduction of ApoB48 which increases ?chylomicron production in consumption of fructose  sakar6 silencing gene CideB which decrease hepatic secretion of small VLDL particles, and a Various ?gene, which regulates LPL including the transcriptional, post-transcriptional, translational protein ?such levels apoC1, apoC2, apoC3, apoA5, angiopoietin-like protein 3 (ANGPTL3), ANGPTL4, ?and ANGPTL8?. . sakar13