lipid transport

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LIPID METABOLISM- Lipid transport and storage:

LIPID METABOLISM- Lipid transport and storage . Dr. Abhijit Gogoi , UNIVERSITY OF FIJI

At the end of this class you ll understand:

At the end of this class you ll understand How lipids are transported in blood between various tissues Lipoproteins Matabolism of different lipoproteins Complications of abnormal lipoprotein metabolism Inborn errors of lipoprotein metabolism

Lipids are transported in plasma as lipoproteins:

Lipids are transported in plasma as lipoproteins Since lipids are hydrophobic they are transported as lipid-protein complexes called lipoproteins The lipid component of lipoprotein contains Triacylglycerols Phospholipids Cholesterol Cholesteryl esters FFA

Classes of lipoproteins:

Classes of lipoproteins Chylomicrons - transport all lipids from intestinal cells Very low density lipoproteins- VLDL- produced in liver to transport TAG Low density lipoproteins- LDL- derived from VLDL High density lipoprotein-HDL

Components of lipoprotein:

Components of lipoprotein TAG and cholesteryl ester surrounded by phospholipid and cholesterol- amphipathic Protein moiety of lipoprotein is apolipoprotein Lipoprotein Apoprotein HDL A LDL B-100 VLDL B-100 Chylomicrons B

Transport of Chylomicrons :

Transport of Chylomicrons Nascent Chlyomicrons , choleterol are produced by the intestinal cells and contain TAG, Apo-B and less quantities of Apo C and E. They are released in to lymphatics . They reach blood. They take up ApoC and E from HDL to become chylomicrons In blood capillaries, Lipoprotein lipase hydrolyzes TAG in chylomicrons to FFA and glycerol. It requires phospholipids and Apo C-II as co factors FFA are taken up by adipose tissue, heart and muscle. 20% goes to liver After 90% TAG and is lost, chylomicron becomes chylomicron remnant which is less in TAG and rich in cholestryl esters and is taken by liver by endocytosis i

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VLDL Nascent VLDL is produced in the liver and contains TAG, cholesterol, B-100,and less quantities of E and C. In blood it takes up Apo C and E from HDL to form VLDL Lipoprotein lipase in the capillary walls digest TAG to form FFA which are taken up by extrahepatic tissues(adipose tissue, heart, muscle and liver). It requires phopsholipids and Apo-C-II as co factor. After losing 90% of TAG, and Apo C,it is called VLDL remnant of IDL(intermediate density lipoprotein), which is rich in cholesterol


LDL Most of the IDL loses all of its TAG by the action of lipoprotein lipase and becomes LDL LDL is rich in cholesterol. It contains B-100 and Apo E 30% of LDL is taken up by extrahepatic tissues and remaining by Liver LDL receptors take up LDL by recognizing B-100 or Apo E.


HDL Is produced in liver and small intestine as discoidal (nascent) HDL. It contains Apo A-1, C, E, cholesterol and phospholipids. ABC-1 transporter in peripheral tissues transports cholesterol from tissues to the HDL. Apo A in HDL binds to Lecithin –cholesterol acyl transferase (LCAT) and the cholesterol and phospholipids are converted into cholesterol esters and lyso lecithin. Now the HDL has more cholesetryl esters and called HDL-3. More Cholesterol is taken up and it becomes HDL-2 HDL-2 binds to SR-2 receptor in liver and is acted upon by hepatic lipase and it removes the cholesterol and it forms HDL 3. this transport of cholesterol from extrahepatic tissues to liver is called Reverse cholesterol transport. HDL-3 takes up cholesterol and form HDL-2, which is called HDL cycle. Old HDL-2 loses A-1 which is destroyed by the kidneys

HDL metabolism :

HDL metabolism Liver SI Discoidal HDL A-1 LCAT PL C Extra hepatic tissues A-1 LCAT Cholesterol C CE PL HDL-3 A-1 C  CE PL HDL-2 C CE PL Hepatic lipase

Clinical applications:

Clinical applications Increased LDL and decreased HDL are predictors of coronary heart disease. LDl when present in high concentrations will get deposited in coronary arteries which will lead to coronary artery diseases like MI, Angina, etc., Lifestyle and diet modifications will reduce LDL and thereby protects from CAD

Dyslipidemias-Freidrickson clasfn :

Dyslipidemias-Freidrickson clasfn Name Defect Result Clinical picture Abetalipoproteinemia Apo- B Chylomicrons , VLDL cannot be formed Fat accumulates in intestine. Fatal Tangier Disease Apo A defect HDL cant be formed Atherosclerosis Familial Lipoprotein Lipase Deficiency (I) LPL defect Slow clearance of VLDL and HDL Harmless Familial Hypercholesterolemia( IIa ) LDL receptor defect  Chol and LDL Atherosclerosis & CAD Familial Type III hyperlipoproteinemia Apo E defect Chylomicrons and VLDL remnants not removed soon  Chol and VLDL, xanthomas , atherosclerosis Familial Hypertriglycerolemia (IV) Glucose intolerance and hyperinsulinemia Overproduction of VLDL  Chol and LDL  CAD Familial Hyper alphalipoproteinemia Increased Apo A production Increased HDL Beneficial to health and long life Hepatic Lipase deficiency TAG rich HDL and VLDL Xanthomas and CAD Familial LCAT deficiency Nascent HDL cannot mature CAD Familial Lp (a) excess Lp (a) is LDL attached with Apo A Early atherosclerosis

Summary :

Summary Chylomicrons  produced in intestine goes to blood delivers FFA to tissues remnant taken up by liver VLDL produced by liver delivers FFA peripheral tissues becomes IDL deliver furthermore FFA becomes LDLtaken up by liver and other tissues HDL reverse chol transport produced by liver takes up Chol from peripheral tissues delivers to liver dyslipidemias

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