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B M B 211 Lecture Notes - Lecture 16: Decarboxylation, Mitochondrial Matrix, Squalene

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coralcrab720
12 Dec 2016
School
PSU
Department
Biochemistry and Molecular Biology
Course
B M B 211
Professor
Giebink Heather

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Document Summary

Cholesterol is derived from the diet or from synthesis in the liver. The liver can make about 900 mg of cholesterol a day. If we take in about 400 mg per day from out diet, synthesis is slowed down. The first steps of cholesterol biosynthesis look exactly like ketogenesis except they occur in the cytoplasm. Acetyl coa comes from the breakdown of glucose. The carbons in the cholesterol chain are coming from acetyl coa. Step 1 is the formation of hmg-coa (1) condensation of two acetyl-coa molecules by a thiolase (2) acetacetyl-coa condenses with another acetyl-coa to form hmg-coa (this is catalyzed by hmg- The rate determining step of cholesterol synthesis and the major control point is the conversion of. Synthetic inhibitors called statins bind extremely tightly to hmg-coa reductase (competitive inhibitors) Lower serum cholesterol levels by blocking synthetic pathway so cells must obtain cholesterol from circulating ldls.

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Related Questions

16- When the body is deficient in oxaloacetate

a) acetyl CoA from the b-oxdiation pathway cannot enter the citric acid cycle

b) oxaloacetate is diverted to gluconeogenesis

c) acetyl CoA is diverted to form the ketone bodies

d) all of the above are true

e) none of the above

17- The synthesis of ketone bodies involves

a) synthesis of acetoacetyl-CoA by reversal of the thiolase reaction of fatty oxidation

b) synthesis of b-hydroxy-b-methylglutaryl-CoA (HMG-CoA)

c) cleavage of HMG-CoA to acetoacetate.

d) b-Hydroxybutyrate is produced by reduction of acetoacetate.

e) all of the above

18- Which of the statements about ketone body production is FALSE?

a) Ketone bodies are produced when there is more acetyl-CoA in the liver than can be oxidized in the citric acid cycle.

b) Ketone bodies production is not a normal process, and occurs only in diabetes or starvation

c) The ketone bodies produced in the body are the free acids and not the CoA esters.

d) When fatty acid oxidation in the liver is uncontrolled, ketone body production becomes excessive and life-threatening because these acidic compounds lower the pH of blood

e) When fatty acid oxidation

19- In which of the following ways can the 4-carbon compound acetoacetyl CoA produced in fatty acid degradation be further metabolized?

a) It can break down further to form acetyl CoA,

b) It can be converted to the ketone bodies

c) It can be used for synthesis of cholesterol and its many deriv­atives.

d) It can do all of the above

e) It can do none of the above

20- Acetyl CoA from the beta-oxidation pathway cannot enter the citric acid cycle in which of these circumstances?

a) periods of fasting

b) periods of starvation

c) diabetes

d) when the body is deficient in oxaloacetate

e) all of the above

30. In final step of the triacylglycerol biosynthesis, which of the following is added to the diacylglycerol?

A. Acetyl-CoA

B. Phosphatidic acid

C. Fatty acyl-CoA

D. Glycerol-3-P

31. The activation of long chain fatty acids requires which of the following?

A. 2 ATPs

B. 2 ATPs and Co-A

C. 2 ATP, CoA and fatty-acyl CoA

D. 2 ATPs and a fatty acid.

32. What is the metabolic pathway that does not involve succinyl-CoA?

A. Ketone bodies to acetyl CoA

B. Odd chain fatty acid oxidation

C. Even chain fatty acid oxidation

D. TCA cycle

33. In order to break down fatty acids, they are first transported into the mitochondrial matrix by conversion of the fatty acid from a covalent complex with CoA to one with:

A. Citrate.

B. Oxaloacetate.

C. Malate.

D. Carnitine.

E. Pyruvate.

34. Regarding carnitine shuttle, the enzyme translocase involves which of the following pair?

A. Fatty acyl & CoA

B. Fatty acyl-carnitine & carnitine

C. Fatty acyl CoA & carnitine

D. Fatty acyl & carnitine

35. The family of drugs that are called "statins" (e.g. lipitor) are effective at lowering plasma levels of cholesterol because they:

A. slow the rate of cholesterol uptake from plasma into the cell.

B. increase the rate of synthesis of cholesterol inside the cell.

C. inhibit the activity of a key enzyme in the cholesterol synthetic pathway.

D. prevent the synthesis of Mevalonate

A 45-year old male goes to the doctor to get his lipid profile done, the results of which are shown below. Using this information and the information from your book, answer the following questions about cholesterol.

Lipid Level(MG/DL)
Total Cholesterol 375
LDL 288
HDL 59

1) What are the types of plasma lipoproteins (name ALL of them)? What is their general role in mammalian metabolism? (2pts)

2) Describe the process by which cholesterol esters in the bloodstream enter cells. (2pts)

3) A co-worker wants to give the patient lovastatin, a potent competitive inhibitor of HMG-CoA reductase. Predict and explain the effect of this drug on serum cholesterol levels in your patient (2pts).

4) Upon further questioning, you discover that his diet and physical levels are normal. Name and describe (briefly) two classes of genetic defects in humans that could produce the blood serum cholesterol profile that your patient exhibits (4pts).