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Biochemistry > Day 5 Cholesterol and Amino Acid Metabolism > Flashcards

Day 5 Cholesterol and Amino Acid Metabolism Flashcards

1
Q

Cholesterol synthesis

A

occurs in the cytoplasm of the liver and only when acetyl CoA is abundant,

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2
Q

Stage 1 of synthesis

A

synthesis of the isopentyl pyrophosphate and activated isoprene units

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3
Q

Stage 2 of synthesis

A

condensation of 6 isooprene to form squalene

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4
Q

Dtage 3 of synthesis

A

formation of tetracyclic sterol ring from squalene and modification to cholesterol.

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5
Q

Ketone bodies

A
  • Degraded to Acetyl CoA in the mitochondria for oxidation.

- Reduced to mevalonate in the cytoplasm for cholesterol synthesis.

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6
Q

Fate of Cholesterol

A

-Cholesterol can produce steroid hormones bile salts and vitamin D

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7
Q

Steroid hormones

A

androgen, testosterone, and estrogen

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8
Q

Vitamin D

A

regulate Calcium absorption and bone metabolism

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9
Q

Bile salts

A

emulsify the dietary fats to allow enzymes to digest them.

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10
Q

HMG CoA reductase

A

Integral membrane protein of the smooth ER that catalyze the committed step of cholesterol synthesis, it is highly regulated. Converts ketone bodies to single acetyl coA units

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11
Q

Regulation of cholesterol synthesis

A
  • Insulin activates synthesis
  • Glucagon inactivates synthesis
  • Low cholesterol activate HMGCoA reductase transcription
  • AMP kinase inactivates HMG-CoA reductase
  • Proteolytic Cleaveactive HMG-CoA reductase transcription
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12
Q

Regulation of Transcription High Cholesterol

A

SREBP is a transactivating protein that induces expression of HMG-CoA reductase and it is kept in the smooth ER membrane inactive when it is bound to SCAP and the levels of cholesterol are high.

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13
Q

Regulation of Transcription Low Cholesterol

A

When the cholesterol levels drop the SREBP complex is cleaved from the ER membrane and goes to the Golgi where it is released from SCAP. SREB is now activated it then travels to the nucleus and increases the transcription of HMG-CoA

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14
Q

Regulation of Translation

A

high cholesterol levels activate mRNA binding proteins that blocks the translation of HMG-CoA reductase.

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15
Q

AMP kinase

A

phosphorylate HMG-CoA reductase and inactivates it due to low energy charge

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16
Q

Cholesterol transport

A

cholesterol and triglycerides are transported via the circulatory system by lipoprotein particles to their respected cell target from the liver and intestines.

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17
Q

Cholesterol Esters

A

Cholesterols are esterified to make it more hydrophobic b ACAT and LCAT

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18
Q

ACAT

A

formation of CE transport from liver to periphery

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19
Q

LCAT

A

formation of CE retrograde transport

inhibited by trans fat

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20
Q

Diateray lipid transport

A

chylomicrons are the lowest density lipoprotein and they are assembled in the intestines to deliver triglycerides to muscle and adipose tissue, the renmants of chylomicrons are returned to the liver to recycle the apolipoprotein.

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21
Q

Synthesized lipid transport

A

do not use chylomicrons. they use VLDL, LDL and HDL to transport the lipids.

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22
Q

IDL

A

intermediate density lipoprotein, precursor to LDL

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23
Q

VLDL

A

transport TG and cholesterol and endogenous fats produced in the liver to peripheral cells. released of the FA transforms them to IDL or LDL via lipoprotein lipase

24
Q

LDL receptors

A

responsible for endocytosis of LDL’s and clearing them from the blood stream.

25
Q

LDL

A

carries mainly cholesterol and Cholesterol esters with Apoprotein B. Binds to LDL receptors triggering endocytocis at peripheral tissues.

26
Q

HDL

A

produced at the peripheral tissue for retrograde transport of cholesterol to the liver

27
Q

Lysosomes

A

degrade LDLs and recycle their component.

28
Q

ABCA1

A

associated with HDLs. it is a cholesterol transported that secretes cholesterol in the blood to be incorporated into HDL.

29
Q

HDL formation

A

HDL are assembled as they collect cholesterol from perpheral tissues. LCAT catalyze the formation of HDL

30
Q

Atherogenesis

A

accumulation of foam cells in the arteries, leading to necrosis, and calcification of the necrotic tissues forms plaques.

31
Q

Foam cell formation

A

oxidation of LDL which cannot be ecndocytosed bi LDL receptors. Macrophages engulf LDLox producing foam cells

32
Q

Paraoxonase

A

HDL associated enzyme that reverses the oxidation of lipids

HDLs prevents the engulfing of LDLs by macrophages

33
Q

Atherosclerosis

A

hardening of the arteries due to accumulation of lipid material in the arteries.

34
Q

Bile acid sequestrants

A

Binds bile salts to the intestines preventing reabsorption of bile acids. Being that it blocks bile acid reabsorption that leads to the intestines increasing bile acid synthesis which competes with cholesterol synthesis. this decrease in cholesterol levels lead to increased production of LDL receptors at the liver.

35
Q

Statins

A

inhibit HMG-CoA reductase to lower the levels of cholesterol and express ion of LDL receptors thereby decreasing the LDL circulation levels

36
Q

Apoprotein B

A

has to do with LDL receptors and cholesterol transport clearance

37
Q

Apoprotein A

A

Regulation of LCAT

38
Q

Apoprotein E

A

triggers clearance of VLDL and chylomicron remnants

39
Q

Apoprotein C

A

regulation of lipoprotein Lipase

40
Q

Proteosome

A

degrades cellular proteins

41
Q

Protein catabolism

A

AA are usually left intact for protein synthesis but can be degraded for energy. degradation of AA occurs in the liver.

42
Q

Amino transferase

A

the first step of protein degradation is to have this enzyme transfer an amino group to alpha ketoglutarate to form glutamate.

43
Q

Ubiquitin

A

signals for protein degradation by proteosome. targets the proteins that needs to be degraded. it has a high degree of specificity

44
Q

Formation of carbomyl phosphate

A

Carbomyl phosphate is the molecule that enters the urea cycle and it is formed from the free ammonia and carbon dioxide.

45
Q

Deamination of glutamate

A

releases free ammonia and regenerates the alpha ketoglutarate

46
Q

Second amino group

A

the second amino group enters as aspartate and that binds to citrulline to form arginosuccinate.

47
Q

Entry into the urea cycle

A

carbamate plus ornithine forms citrulline and that is the addition of the first amino group.

48
Q

Hydrolysis of arginine

A

the hydrolysis of arginine is important because that regenerates ornithine and produces urea for the excretion into the urine

49
Q

Arginosuccinate is cleaved

A

the cleavage of arginosuccinate forms arginine and fumarate this step is important because fumarate replenishes the TCA cycle.

50
Q

Kreb’s bicycle

A

the conversion of OAA to aspartate depletes the TCA cycle however the formation of fumarate from the urea cycle replenishes the cycle

51
Q

Summary of the urea cycle

A

this is a nitrogen excretion pathway. it occurs in the liver and it excretes 2 NH3 per cycle and uses 4 ATP

52
Q

Ketogenic

A

Produces acetyl CoA which cannot be converted to glucose.

53
Q

Glucogenic amino acids

A

most amino acids are glucogenic and they can be used in gluconeogenesis.

54
Q

hyperammonia

A

defects in the urea cycle leading to the accumulation of ammonia in the blood which is neurotoxic

55
Q

Alanine Cycle

A
  • Serves as carbon skeleton for gluconeogenesis. -Some amino acids are deaminated in the skeletal muscle. to get that ammonia to go through the urea cycle in the liver, we transfer it to pyruvate forming alanine which can be transported in the blood and to the liver.
  • Once in the liver, alanine is deaminated and pyruvate goes through gluconeogenesis as glutamate enter the urea cycle.
56
Q

Lipoprotein Lipase

A

Hydrolyzes triglycerides, degrades the triglycerides in lipoproteins and is responsible for the conversion of VLDL to LDL in the bloodstream.

57
Q

arginosuccinase deficiency

A

inactivation of arginosuccinase will lead to the accumulation of arginosuccinate which can be secreted into the urine but the cycle wont be able to regenerate ornithine.

Biochemistry (7 decks)

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