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Flashcards in Lipid Metabolism Deck (28)
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Briefly describe the exogenous lipid pathway

Dietary lipids enter the small intestine and are bound by chylomicrons containing ApoC, ApoE, ApoB-48, etc. and these travel through the intestine where LPL strips free fatty acids (which then go to muscle and adipose tissue).

The smaller remnant chylomicron (atherogenic) then goes to the liver and is taken up via the LDL receptor.


Briefly describe the endogenous lipid pathway

Chylomicron (10:1 TG:CHOL) remnants deliver fatty acids, etc. to the liver where they are re-esterified into TAGs and then packaged into VLDL (5:1 TG:CHOL) containing ApoB-100, ApoE, and ApoC that transports it to the body from the liver.


What is IDL?

Intermediate density lipoprotein (1:1 TG:CHOL) which is made after fatty acids and some cholesterol are stripped off endogenous VLDL. Contains ApoB-100 and ApoE but ApoC has been stripped. This is highly atherogenic as well


What happens to IDL?

it is acted upon by hepatic lipase and the remaining TAGs are stripped leaving a cholesterol rich LDL (less than 5% TAG) molecule.


What is the role of HDL?

to transport cholesterol back to the liver to complete the cycle


What happens if too much LDL is circulating?

some is taken up by peripheral tissue like vessel walls causing atherosclerosis


Write out the Friedewald Formula.

LDL = TC - HDL - TG/5.0 (mg/dL)


What does ApoCII do?

cofactor for lipoprotein lipase (LPL)


What does ApoCIII do?

inhibits LPL so high levels leads to hypertriglyceridemia


What is primary chylomicronemia?

defective removal of CM caused by a apoCII or LPL defect leading to elevated levels of chylomicrons, VLDL elevation, and pancreatitis (common anytime VLDL gets over 1000)


What is the treatment for primary chlyomicronemia?

take the fat out of the diet and replace with medium chain fats that can be broken down without chylomicrons


What is familial hypertriglyceridemia?

defective metabolism of VLDL (LPL defect common) leading to elevated VLDL, pancreatitis, hyperTAG


What is familial dysbetalipoproteinemia?

defective metabolism of VLDL via ApoE defect (activates hepatic lipase) (E2/E2 alleles) in which VLDL can be metabolized to IDL but the IDL then sticks and cant be metabolized

cholesterol and TAG will both be increased


What does familial dysbetalipoproteinemia lead to?

elevated VLDL, IDL, and CM remnants leading to elevated cholesterol and atherosclerosis


How is familial dysbetalipoproteinemia tested?

give the patient a statin which usually lowers LDL but these patients don't have much LDL so nothing happens


What is familial combined hyperlipidemia (FCH)?

overproduction of apoB-100 so VLDL is being pumped out too quick and both VLDL and LDL become elevated leading to premature atherosclerosis





What is familial hypercholesterolemia (FH)? Are TAG levels elevated?

LDL receptor or ApoB defect leading to decreased receptor levels so LDL cannot be cleared effectively leading to high cholesterol

hyperTAGemia is not invariably present (TAGs should be normal here)


What should total cholesterol levels be?

less than 200 mg/dL


What should LDL cholesterol levels be?

less than 130 mg/dL


What should TAG levels be?

less than 120 mg/dL


What should HDL levels be in men? women?

greater than 40 for men
greater than 50 for women


What are some secondary causes of hyperlipidemia?

-kidney disease (nephrotic)
-liver disease (hepatitis, biliary disease)
-simple sugars


Why would nephrotic syndrome lead to hyperlipidemia?

albumin suppresses VLDL production


What kinds of meds could cause hyperlipidemia?

-estrogen (increases TAGs)
-thiazide diuretics


What do high doses of b-blockers and thiazide diuretics do?

block the function of lipoprotein lipase and increase TAG levels


What are the principle dietary factors that increase LDL?

cholesterol and saturated and trans-fats (red meat, dairy products, cheese, pastries, baked goods)


What does HDL do?

binds to ABCG1 transporter on the surface of macrophages and loads cholesterol onto itself and transports it back to the liver in a process called 'reverse cholesterol transport'