- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
![]()
PLAY BUTTON
![]()
PLAY BUTTON
![]()
47 Cards in this Set
- Front
- Back
|
What are the functions of cholesterol?
|
-Inserts in membranes
-Precursor of bile salts -Precursor of steroids -Precursor of vitamin D |
|
Where does the bulk of De Novo cholesterol synthesis occur?
|
LIVER
|
|
How is cholesterol leaving the liver?
|
-Component of HDL's
-Component of VLDL's -Free Cholesterol as bile salts and acids |
|
Where do the carbons used for cholesterol synthesis arise?
|
Acetate, NADPH supplies e-'s
|
|
Where does cholesterol synthesis occur in the hepatocyte?
|
Cytosol and endoplasmic reticulum
|
|
Cholesterol synthesis starts the exact same way that ketone synthesis does with the exception of what?
|
It is occuring in the cytosol of the cell and not the matrix. (2) AcCoA are combined to form Acetoacetyl CoA and then HMG-CoA but in the cytosol. By the enzymes Thiolase, and HMG CoA synthase.
|
|
What is the product of HMG-CoA via the enzyme HMG-CoA reductase in cholesterol synthesis?
|
Hydroxymethyglutaryl CoA ("HMG-CoA")
|
|
What is important about the enzyme HMG-CoA reductase?
|
It is the rate limiting enzyme for cholesterol synthesis and is only found in the liver.
|
|
What inhibits the rate limiting enzyme HMG-CoA reductase?
|
Cholesterol
|
|
Whats important to note about the steps from Mevalonic acid in cholesterol synthesis to squalene?
|
There are many steps, intermediates are phosphorylated, ATP is used to the tune of 7 ~P's, and 1 NADH is consumed (worth 3 ATP)
|
|
How many NADPH's are used in the conversion of HMG-CoA to Mevalonic acid via HMG-CoA reductase?
|
2 NADPH are used, and (1) CoA is released
|
|
What is notable about the conversion of Squalene, a cholesterol synthesis intermediate, to Lanosterol?
|
(1) O2 and (1) NADPH are required, yielding (1) NADP and (1) H2O. Also, the structures from this point on are very hydrophobic and are bound to a carrier protein
|
|
What is the immediate precursor to cholesterol?
|
Lanosterol, there are no remarkable steps Tim would like us to know about this step.
|
|
What are Lovastatin & Metastatin?
|
Anti-Cholesterol (hypolipidemic) drugs that inhibit HMG-CoA reductase (the rate limiting enzyme of cholesterol synthesis)
|
|
Can cholesterol be used for energy? And what is its fate?
|
No, it cannot.
It is used in bile acids, which can be excreted in the feces, or free cholesterol in bile that remains in the feces. -Also, cholesterol can be used to make steroid hormones. |
|
How many classes of steroid hormones are there and what are they?
|
There are 5:
-Glucocorticoids (Cortisol) -Mineralcorticoids (Aldosterone) -Androgens (Testosterone) -Estrogens (Estradiol) -Progestins (Progesterone) |
|
What determines the specific hormone a tissue produces?
|
What enzyme it contains, based on gene expression
|
|
Do both hormones and steroid hormones circulate in the blood freely?
|
Hormones circulate freely in the blood,
Steroid hormones are hydrophobic and are transported in the blood bound to: Albumin, Transcortin (in case of cortisol), and Sex Hormone Binding Protein for the sex hormones. |
|
What is the rate limiting enzyme for steroid hormone synthesis?
|
Desmolase
|
|
What is desmolase?
|
It is the rate limiting enzyme for synthesis of all hormones
|
|
What is the function of desmolase?
|
Converts cholesterol to pregnenolone using (1) NADPH and (1) O2.
|
|
What are the many fates of Pregnenolone?
|
Corticosterone->Aldosterone
Progesterone--->Cortisol Testosterone--->Estradiol |
|
Can steroids be stored?
|
No, steroids are lipid soluble so they would pass through lipid membranes. They are made on-demand and automatically leave endocrine cells.
|
|
What is the "Demand" that is a regulatory polypeptide hormone responsible for stimulating desmolase activity in the endocrine cell?
|
ACTH in the example he gave us, binds the receptor stimulating a 2nd messenger which stimulates Desmolase activity which enzyme converts cholesterol to pregnenolone
|
|
How do steroids alter cell behavior?
|
The alter cell gene expression
|
|
What is the total activity of a protein?
|
Its specific activity multiplied by the amount or # or enzyme molecules
|
|
In addition to becoming steroids, what else can FA's become?
|
Intercellular signals called Eicosanoids (which contain 20 carbons)
|
|
What are eicosanoids?
|
20 carbon unit molecules derived from FA's:
-Prostaglandins -Thromboxanes -Leukotrienes |
|
Why aren't Eicosanoids hormones?
|
They have a short life-expectancy and almost no time to circulate in blood to effect distant tissues/cells.
|
|
What are Eicosanoids also known as?
|
Paracrines. Compounds which aren't steroids or hormones but alter the behavior of neighboring cells. Paracrines are very potents and produced varied responses throughout the body.
|
|
What is an example of an eicosanoid?
|
Arachidonic acid
|
|
What is the precursor of arachidonic acid?
|
Linoleic acid, an essential FA. We also get dietary arachidonic acid.
|
|
What is the source of arachidonate for prostaglandin synthesis?
|
Phospholipids present in our diet.
|
|
Phospholipid in cell membranes is converted to arachidonic acid via which process?
|
Phospholipase A2 cleaves phospholipids yielding Arachidonic acid and a lysophospholipid
|
|
What inhibits the activity of Phospholipase A2?
|
Corticosteroids (cortisol, cortisone)
|
|
What is the fate of arachidonic acid?
|
Converted to 5-HPETE via 5-lipoxygenase
Converted to Prostaglandin G2 (PGG2) via cyclo-oxygenase found in microsomes |
|
What is the fate of 5-HPETE from Arachidonic acid?
|
Becomes Leukotriene A4 and other Leukotrienes
|
|
What is the fate of Prostaglandin G2 (PGG2)?
|
Converted via peroxidase to PGH2, which can then become:
Thromboxane A2 via thromboxane synth. PGI2 (prostacyclin) PGE2--->PGF2alpha |
|
What are leukotrienes?
|
Factors that respond to tissue damage.
|
|
What is the action of leukotrienes?
|
Smooth muscle contract
Bronchoconstriction Slow anaphalaxis Lysosomal release White BC adhesion |
|
What is Thromboxane A2 and its effects?
|
Mostly made by platelets and promote aggregation and vasoconstriction at wound sites.
|
|
What is PGE2 and its function?
|
Most tissues synthesize it but especially the kidney, causes vasodilation and is also used to promote labor.
|
|
What is PGF2 and its function?
|
Made in most tissues. A vasoconstrictor which stimulates smooth muscle and uterine contraction.
|
|
What is PGI2 and its function?
|
Prostacyclin; Primarily made by endothelial cells and causes vasodilation and inhibits platelet aggregation.
|
|
Are cyclo-oxygenase and peroxidase two separate enzymes?
|
No, they are two domains of the same protein complex called prostaglandin synthase
|
|
What inhibits cyclo-oxygenase activity?
|
Aspirin, other NSAIDS, Indomethacin, phenylbutazone. These factors provide their anti-inflammatory effects via this mechanism.
|
|
What does Dipyridamole do?
|
Inhibits Thromboxane synthase, inhibiting thromboxane production without affecting PG's (prostaglandins)
|