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Lipids and Lipoproteins Flashcards

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1
Q

What is precursor for isoprenoids (steroids), lipid soluble vitamins (isoprenoids),& ubiquinone’s?

A

IPP

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2
Q

Sources oAcetyl coa

A

Made in mitochondria: • oxidative decarboxylation of pyruvate Beta ox fatty acids • breakdown amino acids transported into cytoplasm via citrate shuttle

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3
Q

How many IPP units form sterne backbone ring?

A

6

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4
Q

What is alicyclic compound made of?

A

4 fused rings (sterane) W/ one hydroxyl group at c3

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5
Q

What’s most abundant steroid?

A

Cholesterol

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6
Q

T or F: Cells can degrade nucleus of cholesterol

A

False

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7
Q

Biosynthesis of cholesterol is ____ to dietary intake

A

Inversely proportional

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8
Q

How many nadph ATP & Acetyl coa are used for making cholesterol

A

16 nadph 18ATP 18 AcetylCoA

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9
Q

Rate limiting enzyme in cholesterol synthesis 2

A

HMG CoA reductase producing mevalonate & targeted statin, by

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10
Q

Positive regulators of HMG CoA reductase?

A

Insulin & thyroxine

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11
Q

Negative regulators of HMG CoA reductase?

A

Glucagon, sterols, high amp, vitamin E, Statins

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12
Q

What type of inhibition does a statin utilize?

A

Competitive

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13
Q

What is the km for KMG CoA and ki for statins?

A

Km is 4 uM Ki is 5-45 nM

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14
Q

How do statins lead to myotoxic side effects?

A

Statin mediated myopathy from deletion of muscle ubquirone (CoQ10)

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15
Q

What happens with cholesterol In regards to CPR?

A

• Made into ACAT • packed into VLDL

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16
Q

Active form of cholesterol ?

A

Dephosphorylated

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17
Q

How does insulin activate HMG COA reductase

A

Dephosphorylates it

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18
Q

Transcriptional control of HMG CoA Reductase?

A

Binding of TF to promoter

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19
Q

How does low cholesterol impact srebp?

Study These Flashcards
A
  • Triggers translocation of SREBP-SCAP to Golgi
  • SREBP is cleaved & n-terminus released
  • SREBP tf dimer binds to SRE on HMGR promoter
20
Q

Inner core lipoproteins?

Study These Flashcards
A

• Packed W TAGS, cholesterol, cholesterol esters

21
Q

Outer shell lipoproteins?

Study These Flashcards
A

•mono-layer phosphiollpid, free cholesterol, & apolipoproteins

22
Q

Function of lipoproteins?

Study These Flashcards
A
  • Transport & deliver TAGS
  • cholesterol homeostasis
  • Apolipoproteins act as cell targeting signals & ligand
  • lipid metabolism
23
Q

5 types of lipoproteins?

Study These Flashcards
A
  • Chylomicrons (largest, but smallest density, Most TAGs, least protein)
  • VLDL
  • IDL
  • LDL
  • HDL (smallest, but highest density,least TAGs, most protein)
24
Q

Bad cholesterol?

25
Where are chylomicrons formed?
Dietary fats in SI
26
What does ApoB-48 & ApoE &ApoC-II do where are they found?
* ApoB-48 facilitates transport * ApoE facilitates uptake to liver * ApoC-11 activates capillary lipoprotein lipase * chylomicron's
27
Where are VLDL made what are the proteins?
Liver * •ApoB-100: recognized by receptors in target cells * •Apoc-11: activates capilllary lipoprotein lipase * ApoE: promotes heaptic uptake
28
HDL proteins?
* • ApoA-1 activates enzyme to esterify cholesterol * ApoC-11: activates capilllary lipoprotein lipase * ApoE: promotes hepatic upatake
29
IDL proteins?
* ApoB-100 * ApoE
30
What apo proteins are found on a nascent chylomicron?
* ApoB-48: promotes transport
31
What apo proteins are found on the matrue chylomicrons?
* ApoB-48 * Transport * ApoC-II * activates capillary lipoprotein lipase * ApoE * deliver to liver
32
Describe VLDL IDL and LDL processing.
* Start with VLDL and capillary lipoprotein lipase hydrolyzes triacylglycerols to glycerol and free fatty acids. ApoCII is released and IDL remains * IDL gets internalized by liver via ApoE binding hepatocytes. * Hepatic lipoprotein lipase takes off more triacylglycerols and ApoE to become LDL * LDL _deliver cholesterol_ to liver and tissues with binding of ApoB-100
33
Role of LDL? significant Apo protein and core makeup?
* **Major carrier of cholesterol in blood to peripheral tissues and regulates de novo synthesis** * Shell has ApoB-100 which is recognized by receptors in targt cells * Core is packed with 1500 cholesterol esters
34
What causes familial hypercholesterolemia?
* Receptors on LDL are unable to release LDL cargo * Cholesterol in LDL is not used
35
What does LCAT do?
* Gives rise to mature HDL
36
Function of HDL?
* Crucial for maturation of chylomicrons supplies apo C II and ApoE * Scavenges and removes LDL and transports it to liver for processing * "Reverse Cholesterol Transport" brings cholesterol from tissues to liver for excretion
37
What happens when their is a mutation in ABCA1?
* ABCA1 is a cholesterol transport protin in endothelial cells and macrophages * Loss of this results in Tangier disease characterized by HDL deficiency accumulation of cholesterol in macrophages and premature atherosclerosis
38
What cholesterol molecule has antioxidant, anti-inflammatory, antithrombotic, and NO producing properites?
HDL
39
How do you increase HDL-C levels?
* **Weight loss, exercise** and smoking cessation * Antihypercholesterolemic drugs, fibrates, anti-diabetic thiazolidine drugs, estrogens and omega 3 FA
40
What is type I Hyperlipoproteinemia, cause, sx and tx?
* **aka Hyperchylomicronemia** * Inability to hydrolyze TAGs in chylomicrons and VLDL * Caused by a deficiency in Capillary lipoprotien lipase or ApoC-II * Sx: Abdominal pain, acute pancreatitis, cutaneous eruptive xanthomas * Tx: low fat diet (Autosomal recessive)
41
With type I hyperlipoproteinemia what are the two deficiencies that cause it?
* ApoC-II deficiency, post adolescence * Primary LPL deficiency- manifiests in infancy * Plasma TAG levels are greater than 1000 mg/dL
42
What is type II hyperlipoproteinemia, cause, genetics, sx, and tratement?
* **aka familial hypercholesterolemia** * Caused by defects in LDL receptor resutling in defects in uptake of LDL via receptor mediated endocytosis * **inability to recognize ApoB100 on LDL** * Autosomal Dominant * Sx: Xanthomas, corneal eye deposits, angina * Tx: * heterozygous: responds to diet, statins and bile acid binding resins * homozygous: need LDL apheresis and liver transplant
43
In Type II hyperlipoproteinemia (FH), what happens to excess LDL?
* accumulates under endothelial cells lining blood vessesl and undergoes oxidation forming oxLDL * oxLDL initiates inflammatory response deading to development of atherosclerosis
44
With type II FH, what happens with untreated homozygous patients?
* Usually die of CAD Dbefore teenage yeaers
45

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