pathophysiology-of-hyperlipidemia

Pathophysiology of hyperlipidemia : Tryglycerides, and VLDL

pathophysiology-of-hyperlipidemiaPathophysiology of hyperlipidemia : Tryglycerides, and VLDL

Triglycerides are fats, consisting of 3 fatty acid covalently bonded to a glycerol molecule. These fats can be synthesized by the liver, or in the case of those from dietary sources are derived, they are taken up by the liver; triglycerides are transported through the cycle of triglyceride-rich lipoproteins.

Dry weight, so that triglycerides to about 86%, 55% and 23% of chylomicrons, very low-density lipoprotein (VLDL) and intermediate density – lipoproteins (IDL). Triglycerides are low density lipoprotein (LDL) and high density – lipoprotein (HDL), but in much smaller quantities 10% or less.

triglyceride – rich lipoproteins from two sources, often described as endogenously and exogenously. In the exogenous pathway, dietary fats (triglycerides) hydrolyze fatty acids (FFA) and monoglycerides are to release and be absorbed, cholesterol, intestinal cells. They combined with apolipoproteins and phospholipids to form a nascent chylomicrons, a process requires microsomal triglyceride – reesterified transfer protein (MTP). The first apolipoproteins (apo) A, which are soluble and can be transferred to HDL apolipoprotein; and apo B48, a structural apolipoprotein which is not removed during the catabolism chylomicrons. Chylomicrons enter the plasma through the duct, where they acquire other soluble apolipoproteins, including apo CI apo CII, apo CIII, and apolipoprotein E, from HDL.

VLDL and apolipoprotein

VLDL are generated by a method analogous to the exogenous pathway. It can be derived from triglycerides novo – metabolized in the liver and lipoprotein lipase synthesis IDL free fatty acids, also called VLDL remnants. Lipoprotein lipase hydrolyzes triglycerides, releasing FFAs, which are taken up by hepatocytes and myocytes. Some apo Cs, phospholipids and apo es lost and triglycerides are transferred to HDL exchange cholesteryl ester. IDL is therefore cholesterol and triglycerides enriched unmetabolized bad compared to VLDL. As IDL is metabolised by hepatic lipase LDL, the remaining surfaces of apolipoproteins is lost.

Triglycerides can also be derived from the assumption of residual chylomicrons, VLDL or free fatty acids in the plasma. Precursor connects VLDL triglycerides, apo B100 structural or Trans and phospholipids and cholesterol and some apo C and is unripe VLDL formation requires microsomal. – Transfer – protein (MTP). It is once secreted in plasma, VLDL acquire more apo and is Cs and Es.

Keyword for this post :

  • pathophysiology of hyperlipidemia in schematic representation