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GI Tract Biochem > Biosynthesis of Cholesterol > Flashcards

Biosynthesis of Cholesterol Flashcards

1
Q

For what molecules the cholesterol serve as a precursor?

A

Steroid Hormones, Vitamin D and Bile Acids

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2
Q

Excessive cholesterol intake and disorders in cholesterol transport are linked to:

A

Atherosclerosis

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3
Q

Excess of cholesterol in bile lead to:

A

Biliary Stones Formation

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4
Q

Under normal circumstances 30-60% of cholesterol is absorbed in:

A

The Gut

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5
Q

After absorption cholesterol its spread to the liver and peripheral tissues as component of:

A

Chylolmicrons

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6
Q

VLDL and LDL

A

Distribute cholesterol to peripheral tissues

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7
Q

Remove cholesterol from cells

A

HDL

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8
Q

How cholesterol play a role in membrane fluidity?

A

Increase in temperature less fluidity and Decrease in temperature more fluidity

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9
Q

Cholesterol is stratified in cells by:

A

Acyl-CoA: Cholesterol acyltransferase (ACAT)

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10
Q

Cholesterol is stratified in plasma by:

A

Cholesterol-lecithin acyltransferase (LCAT)

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11
Q

Dietary Cholesterol is absorbed from the intestine via:

A

Nieman-Pick C1 protein (NPC1L1)

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12
Q

Secretion of sterols into the bile is mediated by:

A

ATP-Binding cassette G5/G8 (ABCG5 & ABCG8)

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13
Q

Mutations in ABCG5 & ABCG8 results in:

A

Sitosterolemia (accumulation of plants sterols)

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14
Q

Suppress the NPCL1-L1 mediated cholesterol transport and is used in treatment of hypercholesterolemia

A

Eztimibe

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15
Q

Major site of cholesterol synthesis

A

Liver

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16
Q

Provided from the B-oxidation of long fatty acids, Dehydrogenation of pyruvate and ketogenic amino acids

A

Acetyl-CoA

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17
Q

How many moles of Acetyl-CoA, ATP and NADPH is needed to synthesize 1 mole of Cholesterol?

A

18c Acetyl CoA, 36 ATP and 16 NADPH

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18
Q

How begins the biosynthesis of cholesterol?

A

With the condensation of Acetyl-SCoA

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19
Q

Describe the step 1 of cholesterol Synthesis

A

2 molecules of Acetyl-SCoA condense with thiolase to generate Acetoacetyl-SCoA

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20
Q

Describe step 2 of cholesterol synthesis

A

Acetyl-SCoA and Acetoacyl-SCoA are converted to 3-hydroxy-3-methylglutaryl-SCoA synthase by HMG-SCoA Synthase.

21
Q

Describe step 3 of cholesterol synthesis

A

HMG-SCoA is converted to mevalonate by HGM-SCoA reductase.

Completed with NADPH (cofactor for reduction reactions of cholesterol synthesis)

22
Q

Describe step 4 of cholesterol synthesis

A

Mevalonate undergoes a series of phosphorylations and a decarboxylation yielding the isoprenoid, isopentyl pyrophosphate (IPP).

23
Q

Describe step 5 of cholesterol synthesis

A

A series of condensing reactions occur, catalyzed by Squalene Synthase leading to the production of Squalene.

24
Q

Describe step 6 of cholesterol synthesis

A

From Squalene Lanosterol the first of the sterols is formed.

25
Q

Describe step 7 of cholesterol synthesis

A

The conversion of lanosterol to Cholesterol requires 19 additional reaction steps.

26
Q

First Committed Step in the pathway of cholesterol synthesis:

A

Formation of Mevalonic Acid

27
Q

The first two step occur in _______ and are _______ reactions that lead to the formation of:________

A

Cytoplasm, condensation, 3-hydroxy-3- methylglutaryl-CoA (HMG-CoA).

28
Q

Rate limiting enzyme of the byosinthesis of cholesterol is:

A

HMG-CoA reductase

29
Q

The rate-limiting reaction that uses 2 molecules of NADPH and ends with mavealonic acid as product is catalyzed by:

A

HMG-CoA reductase (HMGR)

30
Q

__________ is in the ER and is controlled on multiple levels: by feed back inhibition, degradation rate, phosphorylation (it is active in a nonphosphorylated state), by changes in its gene expression.

A

HGMR

31
Q

It is affected by hormones: insulin and triiodothyronine (T3) increase its activity, whereas glucagon and cortisol inhibit it.

A

HGMR

32
Q

Glucagon promote phosphorylation of the enzyme _________ and cause its ______

A

HGMR, inactivation

33
Q

Insulin promote the desphosphorilation of the enzyme_______ and cause its __________

A

HGMR, Activation

34
Q

HMGR can be phosphorylated (and thus inhibited) by the “energy sensor􏰀” enzyme that is:

A

AMP-dependent kinase (AMPK).

35
Q

Ubiquinone (UQ10), dolichol phosphate, vitamins A, D and K, carotenoids require the formation of:

A

Isopentyl Pyrophosphate

36
Q

Sterol-Sensitive Response Elements (SREs).

A

Mechanism of regulation for LDL receptor and control the expression of all enzymes

37
Q

_________ are found in the promoters of the genes coding for the enzymes of the cholesterol biosynthetic pathway and LDL receptors.

A

SREs

38
Q

Sterol Regulating Element Binding Proteins (SREBPs)

A

Transcription factors important to activating SREs

39
Q

Regulate enzymes in cholesterol synthesis including the rate limiting enzyme HMGR

A

Sterol Regulating Element Binding Proteins (SREBPs)

40
Q

What can happened if the sum of cholesterol synthesized and dietary cholesterol exceeds the amount required for the synthesis of membranes, bile salts, and steroids?

A

Pathological accumulations of cholesterol in blood vessels (atherosclerotic plaques), resulting in obstruction of blood vessels (atherosclerosis).

41
Q

Lovastatin and Compactin

A

Derived from fungi, used to treat patients with hypercholesterolemia.

42
Q

How work lovastatin and compactin?

A

Competitive inhibitors of HMG~SCoA reductase, thus inhibiting cholesterol synthesis

43
Q

Lowers serum cholesterol by as much as 30% in individuals having one defective copy of the gene for the LDL receptor.

A

Lovastatin

44
Q

The bile salts that lack a hydroxyl group at position 7 are called:

A

Secondary Bile Salts

45
Q

Lithocholic acid

A

Secondary bile salt that has a hydroxyl group only at position 3, is the least soluble bile salt, its major fate is excretion.

46
Q

Greater than 95% of the bile salts are resorbed in the ileum and return to the liver via the:

A

Enterohepatic circulation (via the portal vein).

47
Q

Smith-Lemli-Opitz syndrome (SLOS)

A

Characterized by low serum cholesterol levels and elevated 7-dehydrocholesterol levels.

48
Q

Characterized by distinctive facial features, small head size (microcephaly), intellectual disability or learning problems, behavioral problems, autism, malformations of heart, lungs, kidneys, GI tract and genitalia. Weak muscle tone, feeding difficult, slow growing and in most affected cases fused second and third toes (syndactyly), and some have extra fingers or toes (polydactyly).

A

Smith-Lemli-Opitz syndrome (SLOS)

GI Tract Biochem (7 decks)

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