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FCSN 543 – Advanced Nutritional Biochemistry

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									NUTR 543 – Advanced Nutritional Biochemistry
Summer 2007
Exam 2           NAME __________________________________________

1) Chylomicrons function to
   a) Carry cholesterol to extra-hepatic tissues
   b) Carry endogenous triglycerides
   c) Participate in reverse cholesterol transport
   d) Carry dietary triglycerides to peripheral tissues
   e) Synthesize apo-proteins
2) LDLs function to:
   a) Carry cholesterol to extra-hepatic tissues
   b) Carry endogenous triglycerides
   c) Participate in reverse cholesterol transport
   d) Carry dietary triglycerides to peripheral tissues
   e) Synthesize apo-proteins
3) Which of the following processes best describes the events occurring after 1
   week of fasting?
   a) Glucose is the major fuel for skeletal muscle
   b) Ketones are used by the brain for energy
   c) Protein is oxidized by the liver for ATP synthesis
   d) Fatty acids are transported from the liver to adipose
   e) The ratio of insulin to glucagon in the bloo is elevated relative to a 10-hour
      fast
4) HDLs function to:
   a) Carry cholesterol to extra-hepatic tissues
   b) Carry endogenous triglycerides
   c) Participate in reverse cholesterol transport
   d) Carry dietary triglycerides to peripheral tissues
   e) Synthesize apo-proteins
5) Chylomicrons are synthesized in the
   a) Liver
   b) Adipose tissue
   c) Small intestines
   d) Muscle
   e) Kidney
6) A deficiency in Carnitine Acyl Transferase-1 activity in an infant after a 12-
   hour fast would result in:
   a) Ketosis
   b) Hyperglycemia
   c) Acidosis
   d) Accumulation of extra-mitochondrial fats
   e) All of the above
7) VLDLs are synthesized in the
   a) Liver
   b) Adipose tissue
    c) Small intestines
    d) Muscle
    e) Kidney
8) HDLs are synthesized
    a) From IDL
    b) From LDL
    c) In the liver
    d) In fat cells
    e) B and D
9) LDLs are synthesized
    a) From chylomicrons
    b) From VLDL
    c) In the intestinal cells
    d) In adipose cells
    e) From HDL
10) Which of the following enzymes is activated by cAMP-dependent
    phosphorylation?
    a) Acetyl-CoA Carboxylase
    b) Lipoprotein lipase
    c) Hormone-sensitive lipase
    d) Hydroxymethyl-glutaryl CoA reductase
    e) Fatty acid synthase
11) IDLs are NOT:
    a) Largely cleared by extra-hepatic tissues
    b) Made from the degradation of chylomicrons
    c) Taken up by the liver via apo E receptors
    d) Further broken down by hepatic lipase to form LDL
    e) A and B
12) Following a consumption of a snack very high in fat (300 total calories, 75%
    fat) , the lipoprotein that would increase the most one hour after the snack
    would be:
    a) Chylomicrons
    b) VLDL
    c) IDL
    d) LDL
    e) HDL
13) Which of the following is inhibited by malonyl-Co A?
    a) Fatty acid synthase
    b) Acetyl CoA carboxylase
    c) Hormone sensitive lipase
    d) Carnitine acyl transferase-1
    e) Hydroxymethylglutaryl CoA reductase
14) Apoprotein A functions
    a) As a Ligand for LDL-receptors
    b) Activator of lipoprotein lipase
    c) Lipoprotein remnant removal
    d) Reverse cholesterol transport
15) Apoprotein B’s major function is
    a) Reverse cholesterol transport
    b) Regulation of lipoprotein lipase
    c) Remnant recpetor binding and clearance
    d) LDL receptor binding and clearance
16) Which of the following liporoteins would account for most f the plasma
    cholesterol in a 27-yo, healthy man who saw a physician for an annual
    physical examination?
    a) HDLs
    b) Chylomicrons
    c) VLDLs
    d) LDLs
    e) IDLs
17) Which of the following conditions would most likely result in the accumulation
    of cholesterol in extrahepatic tissues?
    a) A deficiency in lipoprotein lipase
    b) A deficiency in acyl CoA: cholesterol acyltransferase
    c) A deficiency in apoprotein A-1
    d) A high level of high density lipoprotein (HDL)
    e) A high level of lecithin-cholesterol acyltransferase (LCAT)
18) Hepatic cholesterol is NOT directly derived from
    a) HDL
    b) LDL
    c) Chylomicron remnants
    d) IDL
    e) De novo synthesis of cholesterol

19) Cholesterol in the liver is NOT removed by
    a) Conversion to bile acids and salts and stored and later excreted in the gall
        bladder
    b) Unesterified cholesterol is secreted as a component of bile
    c) Esterification and packaged into VLDLs and secreted into the blood
    d) Oxidation of the sterol ring and burned as a source of energy
    e) All of the above are ways the liver can remove cholesterol
20) Which drug works to lower blood cholesterol by decreasing the activity of
    HMG-CoA reductase?
    a) Nicotinic acid
    b) Cholestryramine and other bile binding resins
    c) Lovastatin and other statin drugs
    d) None of the above, cholesterol synthesis is regulated by acyl CoA –
        cholesterol acyl transferase (ACAT)
21) When levels of hepatic cholesterol concentrations are elevated (perhaps due
    to chronic consumption of a high cholesterol diet), the following are seen in
    the liver.
    a) Up-regulation of both LDL-receptors and HMG-CoA reductase
    b) Down-regulation of both LDL-receptors and HMG-CoA reductase
    c) Up regulation of LDL-receptors and down regulation of HMG-CoA
        reductase
    d) Down-regulation of LDL-receptors and up-regulation of HMG-CoA
        reductase
22) Which of the following is NOT true with regards to the synthesis of cholesterol
    during feeding.
    a) Increase glycolysis produces more acetyl-CoA and more cholesterol
        synthesis
    b) Increased Pentose phosphate pathway produces more NADPH and more
        cholesterol synthesis
    c) Insulin induces protein phosphatases which converts HMG-CoA reductase
        to an active form
    d) All of the above are true
23) Bile acids and conjugated bile salts differ by:
    a) Conjugated bile salts are better emulsifiers than bile acids
    b) Bile acids are synthesized in the gall bladder whereas conjugated bile
        salts are synthesized in the liver
    c) These terms are synonyms and there are no differences between them
24) The Smith-Lemli-Opitz syndrome is NOT a result of
    a) A deficiency of an enzyme important in the synthesis of cholesterol
    b) A Deficiency of HMG-CoA reductase
    c) Lacking sufficient cholesterol to make myelin in nervous tissue
    d) All of the above
25) Which of the following is operating during prolonged fasting and starvation but
    is not operating in the well-fed state or during an overnight fast?
    a) Fatty acid oxidation in muscle
    b) Fatty acid synthesis in the liver
    c) Triglyceride hydrolysis in adipose tissue
    d) Ketone oxidation in the brain
    e) Triglyceride synthesis in adipose tissue
26) In patients with homozygous familial hypercholesterolemia, describe why
    treatment with bile acid binding resins have little effect on blood cholesterol
    concentration.

Patients with homozygous familial hypercholesterolemia
have no or very low LDL-receptor activity. Bile acid
binding resins reduces the amount of bile acids
reabsorbed in the lower GI tract and forces the body to
synthesize more bile acids from cholesterol. Without
LDL-receptor activity, the liver would not be able to
synthesized more bile acids from LDL-cholesterol (but
would instead stimulate de-novo cholesterol synthesis.
The elevated levels of LDL-C would be unchanged
despite treatment with bile acid binding resins.




27) A 25-yo medical student experienced severe epigastric pain after eating a
    meal containing a large amount of fat. Analysis of plasma apoproteins
    showed a deficiency of apo C. Other apoproteins were normal. Plasma
    elecrophoresis showed an abnormal lipoprotein profile. Which lipoproteins
    would likely be seen elevated in this individual? Explain why these
    lipoproteins would be elevated.

Apoprotein C is required for the activation of lipoprotein
lipase. A deficiency of Apo-C would not allow LPL to
clear chylomicrons from the blood. Marked elevation of
chylomicrons after consuming a high fat meal would
occur as a result of the low LPL activity.
28) Individuals with Type 2 diabetes frequently exhibit elevations of plasma
    triglycerides and free fatty acids. Describe the mechanism by how both of
    these lipids are elevated in Type 2 diabetics.

Type 2 diabetes have impaired insulin sensitivity. Since
lipoprotein lipase activity in increased with insulin, type
2 diabetics have reduced level of this enzyme and are
unable to efficiently clear either chylomicrons or VLDL
resulting in hypertriglyceridemia. Insulin insensitivity
would also result in an increase in activity of adipose
hormone sensitive lipase. Insulin reduces the activity of
HSL by inducing the synthesis of HSL phosphatase
which would inactivate HSL. The resulting elevated
activity of HSL would increase FFA production by
adipose in Type 2 diabetes. In addition, insulin
insensitivity results in lower activity of cAMP
phosphodiesterase and results in higher levels of cAMP
and subsequent activation of HSL.

29) Describe the process by which HDL is involved in the pathway of reverse
    cholesterol transport.

HDL binds to cell membrane receptors and activates
lecithin cholesterol acyl transferase enzymes which
esterify cholesterol in the membranes of peripheral cells
and moves this esterified cholesterol to HDL. The HDL
then transfers these cholesterol esters to IDL and
chylomicron remnants via cholesterol ester transfer
protein. The chylomicron remnants and IDL particles
(VLDL remnants) are removed from circulation by the
liver and ultimately excreted via the bile into the feces.

								
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