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5 lipoprotein metabolism.ppt
- 4. Metabolism of chylomicrons. CM=chylomicron; TAG=triacylglycerol; C=cholesterol; CE=cholesterol esters Reference : Lippincott
- 5. Metabolism of VLDL & LDL TAG=triacylglycerol; VLDL=very low density lipoprotein; LDL=low density lipoprotein; C=cholesterol; CE=cholesterol Reference : Lippincott esters
- 15. Antioxidants Free radicals + - Scavenger receptor Unregulated mechanism for LDL
- 17. Hyperlipoproteinaemias Metabolic defect 1. Type-I (Familial Lipoprotein lipase deficeency) TG Chylomicrone VLDL HDL & LDL Autosomal recessive Lipoprotein lipase 2. Type-II (Familial Hyper- cholestrolaemia) (FHC) LDL T. cholesterol VLDL & TGs Autosomal dominant • Metabolic defect. • Defect LDL catabolism 3. Type-III (Familial dys-beta lipoproteinaemia) LDL VLDL T. cholesterol & TGs Autosomal dominant • Metabolic defect • Apo-E • Defect conversion of VLDL to IDL 4. Type-IV (Familial Hypertriglyceridaemia) (FHTG) VLDL TG synthesis Cholesterol normal/ HDL, LDL Autosomal dominant • Metabolic defect • Tg synthesis • Catabolism of Tg & cholesterol • Glucose intolerence 5. Type-V (Combined Hyperlipidaemia) Chylomicrone & VLDL TGs & Cholesterol HDL & LDL Autosomal dominant -
- 18. Hypolipoproteinaemia Clinical feature Metabolic defect 1.- Lipoproteinaemia (Bassen Kornzweig syndrome) Cholesterol (Absence of LDL) Low Tg conc. No chylomicrone No VLDL • Red blood cell abnormalities. • Malabsorption of fat. • Fatty infiltration. Synthesis of Apo-B 2. -Lipoprotein Deficiency HDL or absent • Hyperplastic orange yellow tonsils Apo-I, II Accumulation of cholesterol esters in different tissu.
- 19. Palmar xanthoma
- 21. Orange yellow tonsil : Tangier disease
Editor's Notes
- Control of plasma LDL production and uptake by liver LDL receptors. (a) In normal human subjects, VLDL is secreted by the liver and converted to IDL in the capillaries of the peripheral tissues. About half of the plasma IDL particles bind to the LDL receptor and are taken up by the liver.The remainder are converted to LDL at the peripheral tissues.
- (c) In normal individuals who have a long-term high-cholesterol diet, the liver is filled with cholesterol, which represses the rate of LDL receptor production. Receptor deficiency, whether of genetic or dietary cause, raises the plasma LDL level by increasing the rate of LDL production and decreasing the rate of LDL uptake.
- (b) In individuals with familial hypercholesterolemia (FH), liver LDL receptors are diminished or eliminated because of a genetic
- Fredrickson’s classification to hyperlipoproteinmias is very important because: 1) They focus on different groups of metabolic abnormalities related to hyperlipoproteinmias. 2) Associated different lipoprotein types with certain clinical features. 3) Provide basis for diet & drug therapy. Lipoprotein disorders may be classified also as: 1- Primary disorder : a) genetic (familial) b- non-genetic (sporadic). 2- Secondary disorder : arise from another cause eg. Diet , alcohol, drugs, or disease of metabolic cause a) hormonal (hypothyroidism , diabetes ) or b) malignant or infectious.