1.A patient presents with skin and tendon xanthomas, a plasma LDL concentration of 375 mg/dl and normal triglycerides. This presentation could result from
a. increased lipoprotein lipase (LPL) activity.
b. a promoter mutation that results in overexpression of acyl CoA: cholesterol acyltransferase (ACAT).
c. decreased synthesis of apolipoprotein B-100 (Apo B-100).
d. increased uptake of oxidized LDL by monocytes/macrophages.
e. a deletion of the exon encoding the signal peptide of the LDL receptor gene.
2.A mutation that inactivates lipoprotein lipase (LPL) would result in
a. increased levels of HDL.
b. increased levels of chylomicrons.
c. decreased ability of hepatic cells to clear LDL.
d. decreased hepatic lipse(HL) present in heparinized plasma.
e. decreased lecithin: cholesterol acyltransferase (LCAT) activity.
3.Phospholipase A2 is important for all of the following EXCEPT
a. release of arachidonic acid for eicosanoid synthesis.
b. release of arachidonic acid to stimulate membrane fusion.
c. repair of oxidized fatty acids in glycerophospholipids.
d. production of dipalmitoylphosphatidylcholine.
e. release of diacylglycerol for activation of protein kinase C
4.Most of our energy reserves are stores as fat because
a. adipose cells have a high biosynthetic capacity to synthesize fatty acids de novo.
b. the energy spent to store glucose as fat is less than that spent to store glucose as glycogen.
c. the recruitment of fat from adipose can be regulated independently of glycogen breakdown.
d. fat is anhydrous and more reduced than carbohydrate.
e. adipose cells have a high level of glycerol 3-kinase activity.
5.Liver cannot utilize ketone bodies for the production of ATP because it lacks the enzyme
b. hydroxymethylglutaryl CoA cleavage enzyme.
c. succinyl CoA:acetoacetate CoA transferase.
d. hydroxymethylglutaryl CoA synthetase.
e. D-3-hydroxybutyrate dehydrogenase.
6.Newly synthesized fatty acids are not immediately degraded primarily because
a. transport of fatty acids into mitochondria is inhibited under conditions in which fatty acids are being synthesized.
b. tissues that synthesize fatty acids do not contain the enzymes that degrade fatty acids.
c. high NADPH levels inhibit beta-oxidation.
d. during synthesis, the key fatty acid degrading enzyme is not induced.
e. newly synthesized fatty acids cannot be converted to their CoA derivatives.
7.Apoprotein A-I (Apo A-I) is an activator of
a. phospholipid transfer protein.
b. lecithin:cholesterol acyltransferase.
c. acyl-CoA: cholesterol acyltransferase.
d. lipoprotein lipase.
e. cholesterol ester transfer protein
8.In the reverse cholesterol transport pathway, cholesterol is transferred to the liver from HDL2 by
a. cholesterol ester transfer protein.
b. a scavenger receptor of the type B family.
c. Apo A-II.
d. phospholipid transfer protein.
e. the LDL receptor.
9.How is HMG-CoA reductase regulated in response to a drop from HIGH to LOW cellular levels of sterols and mevalonate metabolites?
a. Decreased HMG-CoA reductase mRNA transcription.
b. Inhibition of HMG-CoA reductase IThRNA translation.
c. Increased phosphorylation by AMP-activated protein kinase.
d. Increased phosphorylation by cGAMP-dependent protein kinase.
e. Inhibition of proteolysis of HMG-CoA reductase.
10.Which of the following would most likely lead to milky white serum in the fasting state?
a. An excess of lipoprotein lipase
b. A deficiency of Apolipoprotein CII
c. An excess of LDL receptors
d. A deficiency of nascent HDL
e. An excess of lecithin cholesterol acyltransferase (LCAT)