Course Code: BIO 024 (Biochemistry/Biomolecules)

Module #9

Name: ____________________________________________________________ Class number: _______

Section: ____________ Schedule: ____________________________________ Date: _______________

Module 9: CHECK FOR UNDERSTANDING

1. E. Patients with CF, a geneti disease due to a deficiency of functional CFTR, have thickened secretions that impede
the flow of pancreatic enzymes into the duodenum. The acid-stable lipases, lingual and gastric lipase, use as
substrates TAG with short to mediumchain fatty acids that are abundant in milk. Emulsification occurs through
peristalsis that provides mechanical mixing, and bile salts that function as detergents. Chylomicron formation requires
synthesis of the protein apolipoprotein B-48
2. B: TAG in chylomicrons are degraded to fatty acids and glycerol by lipoprotein lipase on the endothelial surface of
capillaries in muscle and adipose, thus providing a source of fatty acids to these tissues for degradation or storage. In
the duodenum, TAG are degraded to 1 monoacylglycerol + 2 free fatty acids that get absorbed. Medium and short chain
fatty acids enter directly into blood; they do not get packaged into chylomicrons. Chylomicrons contain dietary lipids that
were digested and absorbed, thus a defect in fat absorption would result in decreased production of chylomicrons.
3. D: hormone-sensitive lipase is phosphorylated and activated by a cAMP-activated protein kinase.
4. C: TAG-rich chylomicrons are synthesized in (and released from) the intestine following ingestion of a meal. Glucagon
is depressed in the absorptive period. Acetoacetate, free fatty acids, and lactate are not elevated
5. D: Low insulin levels favor the liver producing ketone bodies, using acetyl coenzyme A it generated by β-oxidation of
fatty acids provided by the adipose. Low insulin also causes activation of hormone-sensitive lipase, decreased
glycogen synthesis, and increased gluconeogenesis and glycogenolysis.
6. A: Chylomicrons transport lipids (TAG) absorbed from the intestine to adipose, cardiac, and skeletal muscle tissue,
where their triglyceride components are hydrolyzed by the activity of the lipoprotein lipase, allowing the released free
fatty acids to be absorbed by the tissues.
Chylomicrons are assembled primarily in the intestine and contain a smaller version, apoB-48,
whereas VLDL particles contain the larger apoB-100 surface protein and are primarily assembled in the liver. The
functional role for VLDL and chylomicron particles is to deliver TG to peripheral tissue.
The milky appearance of her plasma was a result of triacylglycerol-rich chylomicrons. Because 5 a.m is presumably
several hours after her evening meal. The patient must have difficulty degrading these lipoprotein particles.
Intermediate-, low, and high-density lipoproteins contain primarily cholesteryl esters, and, if one or more of these
particles was elevated, it would cause hypercholesterolemia. Very-low-density lipoproteins do not cause the described
milky appearance of plasma.

7. C: Liver and intestines. Biosynthesis of Triacylglycerols. Three main pathways for triacylglycerol biosynthesis are
known, the sn-glycerol-3-phosphate and dihydroxyacetone phosphate pathways, which predominates in liver and
adipose tissue, and a monoacylglycerol pathway in the intestines.
8. A: True. Triacylglcerols are stored in the body as cytoplasmic lipid droplets. Within all cell types, even those of the brain,
triacylglycerols are stored as cytoplasmic 'lipid droplets' enclosed by a monolayer of phospholipids and hydrophobic
proteins such as the perilipins in adipose tissue or oleosins in seeds.
9. A: Lipolysis is Hydrolysis of triacylglycerol. Lipogenesis is the formation of lipids. Ketogenesis is the formation of ketone
bodies. Ketolysis is the breakdown of ketone bodies.
10. D: Lipolysis is induced by several hormones, including glucagon, epinephrine, norepinephrine, growth hormone, atrial
natriuretic peptide, brain natriuretic peptide, and cortisol. Insulin signalling enhances lipid storage in adipocytes by both
stimulating triacylglycerol synthesis and inhibiting its breakdown.
11. D. As a result, acetyl-CoA is generated in the mitochondria for oxidation or other possible fates. In the liver, mitochondrial

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 Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #9

Name: ____________________________________________________________ Class number: _______

Section: ____________ Schedule: ____________________________________ Date: _______________

acetyl-CoA is used to synthesize ketone bodies (acetoacetate and β-hydroxybutyrate) as alternative fuel sources for
the brain and heart under conditions of carbohydrate scarcity.
12. B: Ketone bodies (acetoacetate and β-hydroxybutyrate) as alternative fuel sources for the brain and heart under
conditions of carbohydrate scarcity
13. B: ketonemia is a condition where in acetone accumulates in the blood. Whereas ketonuria is when is a medical
condition in which ketone bodies are present in the urine. Ketosis is a process that happens when your body doesn't
have enough carbohydrates to burn for energy. Instead, it burns fat and makes things called ketones, which it can use
for fuel. Ketosis is a word you'll probably see when you're looking for information on diabetes or weight loss
14. C: hormone-sensitive triacylglycerol lipase hydrolyze triacylglycerols stored in adipose tissue. Or the main function of
hormone-sensitive lipase is to mobilize the stored fats . HSL functions to hydrolyze either a fatty acid from a
triacylglycerol molecule, freeing a fatty acid and diglyceride, or a fatty acid from a diacylglycerol molecule, freeing a fatty
acid and monoglyceride.
15. A: Transport of fatty acids from the cytoplasm to the mitochondrial matrix requires: ATP, carnitine, and coenzyme A.
16. B: Fatty acyl–carnitine able to cross the inner mitochondrial membrane.

Fatty acyl CoA is impermeable to the inner mitochondrial membrane, so it is carried in the form of fatty acyl carnitine.

• Fatty acyl carnitine is transported across the inner mitochondrial membrane in exchange for carnitine by an
antiport translocase.
• In the mitochondrial matrix fatty acyl carnitine reacts with CoA in a reaction catalyzed by carnitine acyltransferase
II (CAT-II), yielding fatty acyl CoA and carnitine.

17. C: Order of the enzymes of β oxidation: Acyl-CoA dehydrogenase

- Enoyl-CoA hydratase - β-Hydroxyacyl-CoA dehydrogenase -
Thiolase
18. D: 108
Just follow the computation: like for example for 18C fatty acids yielding
122 ATP.

So for 16C fatty acids”

8 acetyl coA = 80 ATP

This document is the property of PHINMA EDUCATION

 Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #9

Name: ____________________________________________________________ Class number: _______

Section: ____________ Schedule: ____________________________________ Date: _______________

7 FADH2 = 10.5 ATP

7 NADH = 17.5 ATP
Total: 108 ATP

19. B: Ketones :
Ketone bodies (acetoacetic acid, beta-hydroxybutyric acid, and acetone) are insignificant in the blood and urine of
normal individuals in the postprandial or overnight-fasted state. However, these ketoacids become important sources
of metabolic energy in circumstances in which the availability of glucose is restricted, as during prolonged fasting, or
when the ability to use glucose is greatly diminished, as in decompensated diabetes mellitus. During prolonged
starvation the arterial concentrations of these metabolically active strong organic acids increase approximately 70-fold
to 10 to 12 mM and to significantly higher levels of 30 to 40 mM in diabetic ketoacidosis. The mechanisms responsible
for the development of ketonemia are: (1) increased production by the liver; (2) decreased peripheral utilization in
muscle; and (3) reduced volume of distribution. Since ketone bodies are not bound to plasma proteins, they are freely
filterable solutes in the renal glomerulus and appear quantifiably in the tubular urine. At the very low plasma
concentrations of ketone bodies that are encountered normally after an overnight fast, urinary excretion rates are
negligible. When plasma levels increase beyond 0.1 to 0.2 mM, however, excretion increases and measurable amounts
of ketone bodies appear in the urine.

20. A: Ketogenesis occurs primarily in mitochondria of liver cells. Ketogenesis occurs primarily in the mitochondria of liver
cells. Fatty acids are brought into the mitochondria via carnitine palmitoyltransferase (CPT-1) and then broken down
into acetyl CoA via beta-oxidation.

SUGGESTED VIDEOS:
Lipid digestion and absorption: https://www.youtube.com/watch?v=80Edf1o_vDM
Lipid digestion and absorption on the 7th minutes to 9:15th minutes: https://www.youtube.com/watch?v=BVxeeiR7JB0
Lipid metabolism general overview: https://www.youtube.com/watch?v=ppqpUVaasNc
Beta-oxidation Part 1: https://www.youtube.com/watch?v=__jS-pjzb5k
Beta-oxidation Part 2: https://www.youtube.com/watch?v=ZufZvbhPpws
Ketone bodies and ketogenesis: https://www.youtube.com/watch?v=AK9Q2ClI8y4
Lipogenesis: https://www.youtube.com/watch?v=s_sFNG_coSs

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