2 Digestion of Fats

1. In the fed state, how does insulin facilitate the storage of triacylglycerols in adipose tissue?

By inducing the degradation of LDL receptors to prevent cholesterol uptake.
By stimulating the synthesis and secretion of lipoprotein lipase (LPL) from adipose cells.
By activating hepatic triacylglycerol lipase (HTGL) to convert VLDL to LDL.
By inhibiting the transport of glucose into adipose cells to conserve energy.

2. In the process of receptor-mediated endocytosis of LDL, what is the fate of the LDL receptor after the vesicle is internalized?

It is converted into HMG-CoA to regulate cholesterol synthesis.
It is degraded by lysosomal enzymes into amino acids.
It is recycled back to the cell membrane surface.
It remains in the cytosol to act as a storage site for cholesterol esters.

3. Which statement accurately describes the structural organization of a blood lipoprotein particle?

Proteins and phospholipids are covalently bonded to a hydrophobic triacylglycerol backbone.
The density of the particle increases as the percentage of triacylglycerols increases.
Free cholesterol is strictly located in the interior core alongside triacylglycerols.
The core consists of nonpolar lipids like triacylglycerols and cholesterol esters, while the surface is composed of amphipathic phospholipids and proteins.

4. Which apoprotein is described as ‘structural’ and is required specifically for the secretion of VLDL from the liver?

B-100
D
B-48
C-I

5. What is the specific enzymatic action of phospholipase A2 during dietary lipid digestion?

It hydrolyzes the fatty acid at the second (sn−2) position of a phospholipid to produce a lysophospholipid.
It cleaves the ester bond of cholesterol esters in the intestinal lumen.
It removes the phosphate group from the third position of a phospholipid.
It esterifies a free fatty acid onto a lysophospholipid to form a mature phospholipid.

6. Approximately what percentage of dietary fat intake is composed of cholesterol, cholesterol esters, and phospholipids?

2 %
10 %
50 %
90 %

7. Which apoprotein is essential for the uptake of chylomicron remnants and IDL by the liver?

Apoprotein A-I
Apoprotein C-III
Apoprotein E
Apoprotein B-48

8. Where does the re-synthesis of triacylglycerols from 2-monoacylglycerols and fatty acids occur during the absorptive process?

The lumen of the small intestine
The liver sinusoids
The gallbladder
Intestinal epithelial cells

9. What is the primary fate of the cholesterol transferred to VLDL from HDL by the Cholesterol Ester Transfer Protein (CETP)?

It is immediately excreted into the bile by the liver as fecal cholesterol.
It is hydrolyzed by lipoprotein lipase to provide energy for skeletal muscle.
It is eventually delivered to the liver or peripheral tissues as VLDL is converted to LDL.
It is used to synthesize nascent chylomicrons within the intestinal wall.

10. GABA synthesis requires PLP because PLP is required for:

oxidative phosphorylation
decarboxylation reactions of amino acids
methyl group transfer
cholesterol synthesis

11. Why is a high level of High-Density Lipoprotein (HDL) (≥ 60 mg/dL) considered protective against heart disease?

It mediates 'reverse cholesterol transport,' returning excess cholesterol from peripheral tissues to the liver.
It delivers triacylglycerols to adipose tissue for long-term storage.
It inhibits the action of LCAT to prevent the formation of cholesterol esters.
It prevents the synthesis of apoprotein B-100 in the liver.

12. Histamine synthesis from histidine involves removal of which functional group?

hydroxyl group
carboxyl group
amino group
phosphate group

13. How do peripheral cells maintain a constant level of intracellular cholesterol when LDL is taken up?

Cells increase the secretion of apoprotein B-100 to export excess cholesterol as VLDL.
Excess cholesterol is converted into glucose via the gluconeogenic pathway in the lysosomes.
High intracellular cholesterol levels inhibit HMG-CoA reductase and decrease the synthesis of new LDL receptors.
The cells activate LCAT to convert free cholesterol into triacylglycerols.

14. Creatine synthesis requires contributions from arginine, glycine, and methionine primarily because creatine synthesis requires:

ketone body intermediates
methyl group transfer
nucleotide synthesis
bile acid conjugation

15. Which of the following describes the relationship between lipoprotein density and its chemical composition?

HDL has the highest density because it contains the highest percentage of protein and the lowest percentage of triacylglycerol.
VLDL is denser than LDL because it contains more triacylglycerols synthesized in the liver.
Lipoprotein density is determined solely by the amount of cholesterol esters in the core.
Chylomicrons are the densest particles because they carry the largest load of dietary lipids.

16. What happens to the fatty acids and glycerol released by the action of lipoprotein lipase on chylomicrons in adipose tissue?

They are immediately packaged into nascent VLDL particles within the adipose tissue.
Glycerol is used to produce apoprotein B-48 in the adipose cell nucleus.
Fatty acids enter the adipose cells for re-synthesis into TGs, while glycerol is returned to the liver.
Both fatty acids and glycerol are converted into acetyl CoA within the adipose cells for the TCA cycle.

17. Which characteristic distinguishes the activity of lingual and gastric lipases from that of pancreatic lipase regarding substrate specificity?

They catalyze the complete hydrolysis of triacylglycerols into three free fatty acids and one glycerol molecule.
They exhibit an optimal catalytic pH of approximately 7.0 to 8.0.
They primarily target triacylglycerols containing short-chain and medium-chain fatty acids (≤ 12 carbons).
They require the presence of co-lipase to function within the acidic environment of the stomach.

18. Which enzyme, located on the surface of endothelial cells, is responsible for the hydrolysis of triacylglycerols in VLDL and IDL?

Pancreatic lipase
Hepatic triacylglycerol lipase (HTGL)
Cholesterol esterase
Gastric lipase

19. What is the primary physiological function of pancreatic co-lipase during intestinal lipid digestion?

To anchor pancreatic lipase to the surface of lipid emulsion particles in the presence of bile salts.
To facilitate the re-esterification of 2-monoacylglycerols within the intestinal epithelial cells.
To directly hydrolyze cholesterol esters into free cholesterol and fatty acids.
To activate the deprotonation of bile acids into their anionic salt form.

20. The deprotonated form of bile acids, known as bile salts, is effective in digestion because of what property?

Enzymatic hydrolysis
Acidic pH stabilization
Antioxidant activity
Detergent properties

21. The action of pancreatic lipase on a triacylglycerol molecule specifically results in which of the following product sets?

Glycerol and three free fatty acids.
Lysophospholipid and a cholesterol ester.
2-monoacylglycerol and two free fatty acids.
1,2-diacylglycerol and one free fatty acid.

22. Which apoprotein is the primary activator of the hepatic lipase enzyme?

B-100
A-I
A-II
C-II

23. Which component is essential for the formation of mixed micelles in the intestinal lumen to facilitate the absorption of lipid-soluble vitamins?

Lipoprotein lipase
Albumin
Bile salts
Apoprotein B-48

24. What distinguishes ‘nascent’ chylomicrons from ‘mature’ chylomicrons?

Nascent chylomicrons lack apoproteins C-II and E, which they later acquire from HDL in the blood.
Mature chylomicrons contain only short-chain fatty acids synthesized in the liver.
Nascent chylomicrons are produced in the liver, while mature ones are found in the lymph.
Mature chylomicrons have a higher triacylglycerol-to-protein ratio than nascent ones.

25. Apoprotein B-48 is a critical structural component of which lipoprotein particle, and where is it synthesized?

LDL; synthesized in the blood plasma.
VLDL; synthesized in liver cells.
HDL; synthesized in both the liver and intestine.
Chylomicrons; synthesized in intestinal epithelial cells.

26. If a patient has a genetic deficiency in Apoprotein C-II, what would be the expected clinical finding?

Abnormally low levels of LDL due to rapid conversion of VLDL.
Markedly elevated levels of chylomicrons and VLDL in the plasma.
Total absence of cholesterol in the peripheral tissues.
Inability to absorb lipid-soluble vitamins from the intestinal lumen.

27. Which enzyme is responsible for the esterification of cholesterol within the blood plasma to form mature HDL particles?

Hepatic triacylglycerol lipase (HTGL)
Lecithin-cholesterol acyltransferase (LCAT)
AcylCoA: cholesterol acyltransferase (ACAT)
Lipoprotein lipase (LPL)

28. The conversion of dietary cholesterol esters into free cholesterol in the gut is catalyzed by which enzyme?

Lingual lipase
ACAT
Cholesterol esterase
LCAT

29. What role does apoprotein C-II play in the metabolism of chylomicrons and VLDL?

It serves as the primary ligand for the LDL receptor in peripheral tissues.
It inhibits the premature removal of triacylglycerol-rich lipoproteins by the liver.
It acts as a necessary activator for lipoprotein lipase (LPL) in the capillaries.
It mediates the exchange of cholesterol esters for triacylglycerols via CETP.

30. Which of the following is a byproduct of the lipoprotein lipase (LPL) reaction?

Bile acid
Glycerol
Mevalonate
2-monoacylglycerol