FAs, Lipids, and Cholesterol Flashcards Preview

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Flashcards in FAs, Lipids, and Cholesterol Deck (50)
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Stimulation of HMG CoA Reductase Activity (2)

Phosphoprotein phosphatase dephosphoactivates it
SREBP also binds SRE, stimulating transcription of HMG CoA Reductase


Inhibition of HMG CoA Reductase (2)

AMPK phosphodeactivates
Cholesterol inhibits SREBP release from Golgi


Statins Action

Lower cholesterol my inhibiting HMG CoA Reductase


Bile Acid Synthesis

Cholesterol 7-alpha-hydroxylase adds carboxylic acid to cholesterol alkane tail to for cholic acid or chenodeoxycholic acid


Bile Salt Synthesis (2)

Glycine added to cholic acid to make glycocholic acid
Taurine added to chenodeoxycholic acid to make Taurochenodeoxycholic acid


Enterohepatic Circulation

Bile salts/acids sent from liver/gallbladder to intestines and those that aren't excreted are recycled back to liver


Steroid Synthesis (7 different molecules mentioned total)

Cholesterol to pregnenolone to progesterone which differentiates into cortisol, aldosterone, or testosterone (and then estradiol from there)


Congenital Adrenal Hyperplasias (CAH)

Deficiencies in enzymes along the steroid hormone synthesis pathway


General Passage of Cholesterol Through Lipoproteins (5)

Chylomicrons w/ lots of TAGs go from GI to muscles/tissues
Remnants go to liver
Contents repackaged into VLDL w/ some TAGs and cholesterol which goes to tissues
LDL returns to liver w/ just cholesterol and cholesteryl esters
HDL then secreted in bile, takes up cholesterol from peripheral tissues and returns


Lipoprotein w/ Highest TAG component



Lipoprotein w/ Highest Cholesterol Component



Chylomicron Apolipoproteins (3 prots, 5 points)

Apo B-48 added upon nascent in SI
Then C-II and Apo E added from HDL
C-II activates lipoprotein lipase to hydrolyze TAGs to FAs and glycerol in capillaries
Then Apo C-II returned to HDL from remnant
Apo E binds to Rs in liver for endocytosis of the remnant


VLDL and LDL Apolipoproteins (3 prots, 5 points)

Apo B-100 on nascent VLDL in liver
Then Apo C-II and Apo E added from HDL
Apo C-II activates lipoprotein lipase to hydrolyze TAGs to FAs and glycerol in capillaries
Apo C-II and Apo E returned to HDL from LDL (which now has CEs and C almost entirely)
Apo B-100 binds to LDL Rs on extrahepatic/liver tissues and are endocytosed


Cholesteryl Ester Transfer Protein (CETP)

Catalyzes transfer of TAGs to HDL from VLDL and CE from HDL to VLDL


Difference b/w Apo B-100 and Apo B-48

Come off same gene w/ same mRNA, but a cytosine is edited in ssRNA to create a stop codon to make Apo B-48 for chylomicrons


Familial Hypercholesterolemia

Low LDL Rs causes hypercholesterolemia



Gene for LDL R degrading protein on outside of the cell, new even more effective target for inhibition decreasing cholesterol


2 Inhibitory Effects by Cholesterol

Blocks HMG CoA Reductase
Blocks synthesis of LDL Rs


Cholesterol's Contribution to Arterosclerosis (major point and 4 steps)

Individual has to have high cholesterol *AND* unknown susceptibility to oxidative
Endothelium causes/releases oxidative stress
LDLs damaged by it
Macrophages swallow damaged LDLs and become foam cells
Foam cells deposit onto arterial walls causing plaques


HDL Circulation

Released as bile and then has intermediate stages which pick up cholesterol from peripheral tissues and return to liver