Set 5 Cholesterol Synth And Reg

Front 1

What defines a steroid?

Back 1

a molecule with 3, 6 carbon rings adjacent to each other, attached to an additional 5 ring carbon.

Front 2

Cholesterol is a precursor for:

Back 2

Steroid hormones, and bile salts.

Front 3

What is cholestor used for?

Back 3

a cell membrane component, bile salt and steroid hormone precursor, precursor for vitamin D

Front 4

Where do all of the carbons for cholesterol come from?

Back 4

Acetyl CoA

Front 5

Where does Cholesterol synth occur within the cell, and within the body?

Back 5

Cholesterol synth is primarily in the liver, and it takes place within the ER.

Front 6

What is the committed step in Cholesterol synthesis, and which enzyme regulates this step?

Back 6

The production of Mevalonate, regulated by HMG-CoA reductase.

Front 7

Which hormone promotes the production of mevalonate from HMG-CoA (helps activate HMG-CoA)

Back 7

Insulin. HMG CoA is active when blood sugar is high, therefore Cholesterol is produced when blood sugar is high.

Front 8

Which hormones indirectly inhibits HMG CoA reductase?

Back 8

Glucagon, oxysterol and AMPK will inhibit HMG-CoA reductase by phosphorylating it under conditions with high [AMP]

Front 9

Where is Cholesterol Made, and where are Ketone bodies made?

Back 9

Both in the liver, however, Cholesterol is made in the cytosol, whereas Ketone bodies are made in the Mitochondrial matrix.

Front 10

When is cholesterol made, compared to when ketone bodies are made?

Back 10

Cholesterol is made during times of plenty, and Ketone bodies are made during starvation.

Front 11

Which molecule on the ER is a sensor for sterol?

Back 11

SCAP (SREBP Cleavage-activating protein) , when bound to sterol, prevents the cleavage of SREBP (Sterol regulatory element binding protein)

Front 12

When cholesterol levels are low in the cell, what happens to SCAP

Back 12

If sterol is not bound to SCAP, SCAP will cleave SREBP, releasing a N terminus of the SREBP protein, which will go to the nucleus of the cell, and act as an inducer for the HMG reductase gene. It will increase transcription of the HMG reductase gene.

Front 13

Order from biggest to smallest, HDL, Chylomicrons, VLDL, LDL.

Back 13

Chylomicrons, VLDL, LDL, HDL

Front 14

In which cell type are chylomicrons produced?

Back 14

Enterocytes (small intestine cells

Front 15

_____ activates ______ released FAs from TAGs in chylomicrons into tissues

Back 15

ApoC-II activates Lipoprotein Lipase

Front 16

What happens to excess Fatty acids and cholesterol from the diet?

Back 16

THey get incorporated into VLDL

Front 17

Which receptor is expressed on cells that signals it is in need of cholesterol, and what type of Apolipoprotein does it bind it?

Back 17

LDL receptor. Apolipoprotein B 100

Front 18

How is cholesterol stored in VLDL and LDL

Back 18

Cholesterol is stored in a single layer, beside the phospholipids at the surface of the lipoprotein, with it's hydroxy group facing out. Inside of the lipoprotein, cholesterol is stored as a cholesterol ester (as the ester form is completely hydrophobic).

Front 19

What is IDL?

Back 19

Intermediate density lipoproteins. Formed after VLDL releases some TAGs, but still has more TAGs than LDL.

Front 20

HDL goes from _____ to ______.

Back 20

Extrahepatic tissues to the Liver.

Front 21

Why type of cholesterol modifying enzyme does HDL contain?

Back 21

Cholesterol esterase.

Front 22

What is the fate of cholesterol that goes to the liver?

Back 22

It gets turned into bile salts, and the bile salts are stored in the gall bladder.

Front 23

which type of lipoprotein has the most protein?

Back 23

HDL

Front 24

What happens if there are no/malfunctioning LDL receptors.

Back 24

Increased concentrations of cholesterol in the blood (Hypercholesteremia). Since the concentrations in the blood are higher, the cholesterol will remain there longer, so it will have a higher chance of becoming oxidized. If Cholesterol is oxidized, it will become stuck to the extracellular matrix. Macrophages will then engulf the cholesterol, and become foam cells. Once a certain threshold of cholesterol is engulfed, the foam undergo apoptosis, and the remnants will be released. Over time this plaque accumulates

Front 25

what constitutes the plaque in atherosclerosis?

Back 25

Foam cell remnants, extracellular matrix, and smooth muscle tissue.

Front 26

Why is HDL good?

Back 26

Because it takes Cholesterol to the liver, and not the blood, where it used to make bile salts.

Front 27

What are the four stages of Cholesterol synth?

Back 27

Acetyl-CoA --> mevalonae --> activated Isoprene --> squalene.