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 After a meal, chylomicrons that are triglyceride-rich lipoproteins
(TRL) produce and export from enterocytes into lymph before transporting to the
circulation subsequently, chylomicrons hydrolyzes by Lipoprotein lipase (LPL)
into fatty acids that provide energy to the heart and skeletal muscles or
stored in adipose tissue. Chylomicron remnants are removed from the circulation
after binding to the LDL receptor


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    However, the excess TG after a meal rich in
dietary fat temporary store in cytoplasmic lipid droplet (CLDs) to prevent lipotoxicity

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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 ?


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. 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 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?.