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Biochem 2 (SW) > Final > Flashcards

Final Flashcards

1
Q

What 2 things cause the regulation of fa synthesis?

114

A

Acetyl-CoA Carboxylase.

Malonyl-CoA. (-)

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2
Q

What 3 things activate Acetyl-CoA Carboxylase?

114

A

Citrate: means that large amounds of OA and acetyl CoA are present and it’s a good time for fa synthesis. (Decrease of OA or acetyl-CoA will decrease fa synthesis).
Insulin: Secreted in response to a meal (pancakes)
Increased CHO, decreases fat

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3
Q

What inhibits Acetyl-CoA Carboxylase?

114

A

Palmitoyl-CoA: Feedback mechanism.

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4
Q

After fa synthesis, what happens to the fatty acids?

115

A 
Triglycerides:  adipocytes -> storage; Liver -> VLDLs; Small intestines -> Chylomicrons. 
Phosphoglyceride synthesis (nonpolar):  Lipid bilayer of all cells.
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5
Q

Where does cholesterol metabolism take place?

119

A

Mostly in the liver (and small intestine).

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6
Q

As cholesterol intake increases, what happens to feedback regulation?

(119)

A

Feedback regulation decreases production.

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7
Q

What are the 3 main things cholesterol is turned into?

119

A 
Progesterone (gluco-corticoids, mineralocorticoids, androgens, and estrogen).
Vitamin D (UV light at the skin).
Bile Acids (made in the liver).
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8
Q

Explain cholesterol biosynthesis:

120

A

Start with acetyl CoA –> HMG-CoA –> (HMG-CoA reductase) Mevalonate –> Active Isoprene… –> Cholesterol.

Overall: 18 acetyl-CoA’s, 6 Isoprene units, 18 ATP’s, 16 NADPH’s (from pentose shunt)

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9
Q

What is the key regulatory enzyme for cholesterol biosynthesis?
Is it long term or short term?

(121)

A 
HMG-CoA reductase.
Long term (hours, days).
(Increased dietary cholesterol intake --> decreased HMG-CoA reductase levels, through enzyme degradation).
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10
Q

What regulates the short term cholesterol biosynthesis?

121

A

Phosphorylation: Inactive

De-phosphorylation: Active

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11
Q

What is the competitive inhibitor of HMG-CoA reductase?

121

A

Statins.

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12
Q

What are the 3 options for cholesterol turnover in the liver?

(122)

A

Excreted.
Converted to bile acids.
Turned into VDLD’s.

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13
Q

What are the 3 types of plasma/serum lipids?

123

A

Triglycerides.
Phospholipids.
Cholesterol (Cholesterol esters of f.a.)
(Lipids are pachaged with proteins to give a lipoprotein complex).

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14
Q

What are the reasons for transport of lipids?

123

A

Move to peripheral tissues (away from liver).
Transport of dietary lipids.
Excretion of cholesterol in bile.
Release of free fatty acids during mobilization.

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15
Q

What does VLDL represent?
How is it affected with CHO increase?

(125)

A

Represents transport of lipids from the liver to other tissues, especially adipose.
VLDL increases with CHO in the diet.

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16
Q

What does the deposit of tg in the tissues require?

125

A

LDLase.

17
Q

What is most serum cholesterol associated with?

125

A

LDL’s

18
Q

Where are HDL’s synthesized?

126

A

Liver.

Prevents excess cholesterol accumulation and is thought to remove excess cholesterol (requires LCAT enzyme).

19
Q

What do chylomicrons do?

126

A

Carry dietary fats.

~1 hour for overall processing

20
Q

Where are chylomicrons formed?

126

A

Within the mucosa cells.

They go through the lymphatics and enter the blood via the thoracic duct.

21
Q

What does serum albumin do?

126

A

Carries free fatty acids (primarily those released from adipose in mobilization).
These aren’t directly measured as blood lipids (some ffa’s go to the liver and are packaged into VLDL and then go to the blood).

22
Q

What binds bile acids and cholesterol?

127

A

Fiber.

23
Q

What is the path for the transport of lipids from the liver?

(128)

A

Liver –> VLDL –> LDL –> Extrahepatic tissue LDL r/c

Familial Hypercholesterolemia involves decrease LDL r/c

24
Q

What are the 2 hormones that act on own r/c’s?

129

A

Epinephrine.

Glucagon.

25
Q

Is a fatty liver reversible?
How does a fatty liver happen?

(133)

A

It is reversible.
There is usually a balance b/w VLDL synthesis and VLDL’s released into the blood. If the equilibrium is altered, tg’s get deposited in the liver. –> cell damage, scarring, and eventually cirrhosis.

26
Q

What is the effect of excess ethanol intake?

133

A

Decreased gluconeogenesis –> hypoglycemia b/c the lactate to pyruvate step is prevented.

27
Q

What are the 4 pathways for amino acid metabolism?

134

A

Protein Synthesis: ~75% of amino acids.
Synthesis of non-protein nitrogen compounds (NPN).
Energy utilization (oxidation): Removal of nitrogen; oxidation of carbon skeleton.
Synthesis of non-essential amino acids.

28
Q

Which amino acid pathway is catabolic?
Anabolic?

(134)

A

Catabolic: Energy utilization.
Anabolic: Synthesis of non-essential amino acids.

29
Q

What 2 things increases our dependence on amino acids as an energy source?

(135)

A

Increased protein intake.

Decreased CH2O intake –> a.a. used in gluconeogenesis.

30
Q

During amino acid catabolism what are the 3 ways we utilize the c-skeleton?

(135)

A

Oxidation in the citric acid cycle.
Conversion to glucose (gluconeogenesis).
Conversion to fat (via acetyl-CoA).

31
Q

What is the usual excretion molecule for nitrogen?

135

A

Urea.

32
Q

What does removal of an amino group from amino acids require?

(135)

A

Transamination.
Oxidative Deamination.
Urea Synthesis (Urea cycle).

33
Q

What is the alpha keto acid for glutamate?
Aspartate?
Alanine?

(136)

A

Glutamate: Alpha Ketoglutarate (K.C. Int.)
Aspartate: Oxaloacetate (K.C. Int.)
Alanine: Pyruvate (Glycolysis Int.)

34
Q

With respect to urea synthesis, where is transamination most important?

(137)

A

Liver.

35
Q

Transamination serves as a means of…:

137

A

Means of Interconverting amino acids: allows cells to shuffle the amino acid pool.
Means of shuttling NH3+ groups to glutamate and aspartate (which sets things up for entry into the urea cycle).

36
Q

What are the 3 features of transaminases?

137

A

Always include alpha ketoglutarate and glutamate.
Pyridoxal phosphate.
/_\G’ ~0 (equilibrium ~ equal).

37
Q

What are the products of oxidative deamination of Glutamate?
Alanine?
Aspartate?

(139)

A

a.a. –> alpha keto + NH4+
Glutamate: Alpha ketoglutamate + NH4+
Alanine: Pyruvate + NH4+
Aspartate: Oxaloacetate + NH4+

38
Q

What are the 2 ways a.a.’s lose thier amino groups when catabolized?

(141)

A

Transamination.
Oxidative deamination.
(Ultimately Nitrogen is excreted primarily as urea).

Biochem 2 (SW) (2 decks)

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