BIO3101 CONFIDENTIAL

SULIT

UNIVERSITI MALAYSIA TERENGGANU

ALTERNATIVE FINAL ASSESSMENT

PENILAIAN AKHIR ALTERNATIF

SEMESTER II 2020/2021 SESSION (DEGREE PROGRAMME)

SEMESTER II SESI 2020/2021 (SARJANA MUDA)

COURSE : BIOCHEMISTRY
KURSUS BIOKIMIA

COURSE CODE KOD : BIO3101

KURSUS
DATE : 25 JULAI 2021 (AHAD) – 29 JULY 2021 (KHAMIS)
TARIKH 25 JULY 2021 (AHAD) – 29 JULY 2021 (THURSDAY)
VENUE : OCEANIA E-LEARNING
TEMPAT
TIME : -
MASA

MATRIC NO. : S56094__________________________________________

NO. MATRIK

PROGRAMME : BIOLOGICAL SCIENCE______________________________

NAMA PROGRAM

SEAT NO. : ______________________________________________

NO. MEJA

INSTRUCTIONS TO CANDIDATES
sE
ARAHAN KEPADA CALON

i. Answer ALL questions.

Sila jawab SEMUA soalan.
ii. All answers must be typed, digitally drawn (except the snapshot required) and
submitted in .pdf format.
Semua jawapan hendaklah ditaip, dilukis secara digital (kecuali gambar yang diminta)
dan dihantar dalam format .pdf.

DO NOT OPEN THE QUESTION PAPER UNTIL INSTRUCTED

JANGAN BUKA KERTAS SOALAN INI SEHINGGA DIBERITAHU

THIS QUESTION PAPER CONSISTS OF TWO (3) PRINTED PAGES

KERTAS SOALAN INI MENGANDUNGI DUA (3) MUKA SURAT BERCETAK

THIS ASSESSMENT HAS THREE (3) QUESTIONS. ANSWER ALL QUESTIONS.

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PENILAIAN INI MENGANDUNGI TIGA (3) SOALAN. JAWAB SEMUA SOALAN.

1. Identify one raw food sold in the local market or online shopping app that become
the source of essential amino acids to human.

i- Take a snapshot of the raw food.

What is the common name of the food?
List the essential amino acids contained in that raw food.

Quinoa is the common name for Chenopodium quinoa.

Quinoa is a complete protein, which means it includes all nine
essential amino acids that our systems are unable to produce on their
own which are histidine, isoleucine, leucine, lysine, methionine,
phenylalanine, threonine, tryptophan, and valine. [5M, C3]

ii- Match the enzymes produced by our body that are responsible for the
degradation of the essential amino acids listed in (i).

 Histidine- Histidase, Glutamate dehydrogenase

 Isoleucine- Isobutyryl-CoA dehydrogenase
 Leucine- Isovaleryl-CoA dehydrogenase (IVD)
 Lysine- Alpha aminoadipic semialdehyde synthase
 Methionine- Methionine adenosyl transferase
 Phenylalanine- Phenylalanine hydroxylase (PAH)
 Threonine- Threonine-3-dehydrogenase(TDH)
 Tryptophan- Tryptophan 2,3-dioxygenase(TDO)
 Valine- Isobutyryl-CoA dehydrogenase [8M, C4]

iii- Illustrate in a simplified flow diagram how these essential amino acids
obtain their nitrogen from the environment.
[7M, C4]

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2. (a) Generous amount of olive oil is consumed by people who live in Mediterranean
countries. People at high risk for cardiovascular disease who followed the
Mediterranean diet had fewer major cardiovascular events than those who
followed a reduced-fat diet.

i) List the types of fatty acids present in olive oil. [3M]

Saturated fatty acids

 Stearic acid
 Palmitic acid
 Behenic acid
 Lignoceric acid

Unsaturated fatty acids

 Oleic acid (monounsaturated)
 Linoleic acid (polyunsaturated)
 Linolenic acid (polyunsaturated)

ii) Describe how the fatty acids in olive oil affect the fate of cholesterol in the
cells which in turn reduce the risk of cardiovascular disease. [6M]

Unsaturated fatty acids like oleic acid, linoleic acid, and linolenic acid are the
most abundant in olive oil, followed by saturated fatty acids like stearic acid
and palmitic acid in lesser amounts. Olive oil, which is high in
polyunsaturated fatty acids (PUFAs) like alpha-linolenic acid (ALA) and

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linoleic acid (LA), lowers cholesterol levels by converting PUFA into ketone
bodies rather than very low-density lipoprotein (VLDL) triglycerides, which
lowers blood VLDL and LDL concentrations. PUFAs, unlike saturated fatty
acids, are transported to tissues for oxidation without leaving any lipoprotein
residues in the form of LDL. In this context, PUFAs effectively reduce
inflammatory markers to prevent heart disease, specifically the inflammatory
processes that contribute to cholesterol deposition inside the arterial wall
and plaque development (atherosclerosis).

The most abundant monounsaturated fatty acid (MUFA) in olive oil, oleic
acid, lowers LDL cholesterol. In addition, oleic monounsaturates have a
better effect on lipoproteins, which can increase triglycerides and lower HDL
cholesterol levels. High blood cholesterol levels are known to induce clogged
arteries and heart attacks, which are risk factors for cardiovascular disease.
Monounsaturated fat consumption is linked to reduce blood cholesterol
levels. In a nutshell, MUFA appears to hold greater promise in cholesterol-
lowering diets. In a nutshell, PUFAs and MUFAs are responsible for reducing
inflammation and coronary thrombosis.

(b) Describe how acetyl CoA accumulation can influence the cascade of ATP
production, ketogenesis and lipogenesis [8M].

Acetyl-CoA is a metabolite formed when glucose, fatty acids, and amino acids
are broken down. Pyruvate, a product of glycolysis, is converted to acetyl CoA
in the mitochondria in the following phase. In a sequential process, the citric
acid cycle absorbs the energy contained in the chemical bonds of acetyl CoA
and traps it in the form of high-energy intermediate molecules. The trapped
energy from the citric acid cycle is subsequently transferred to oxidative
phosphorylation, where NADH and FADH2 are delivered to the electron
transport chain, boosting ATP generation with their high-energy electrons.

When the Krebs cycle becomes overloaded with acetyl CoA produced by fatty
acid oxidation, it is shifted to the ketogenesis pathway, where it is transformed
to ketone bodies in the mitochondria. These ketone bodies can be used as a
fuel source if the body's glucose levels are too low. Ketones are used as a source
of energy during prolonged fasting or when individuals with uncontrolled
diabetes are unable to use the majority of the circulating glucose. In both cases,
fat stores are released to provide energy via the Krebs cycle, and ketone
molecules are formed when too much acetyl CoA accumulates.

When too much glucose or carbohydrate is taken, accumulated acetyl CoA can
be used for fatty acid synthesis or lipogenesis. Acetyl CoA is produced during
glycolysis and is utilised to generate lipids, triglycerides, steroid hormones,
cholesterol, and bile salts. Lipogenesis is a process in which adipocytes and
hepatocytes synthesise lipids from acetyl CoA in their cytoplasm. During
lipolysis, triglycerides are broken down into glycerol and fatty acids, making
them easier to digest. Acetyl CoA is used to convert extra glucose or
carbohydrates into fat when you consume more than your body requires.
Lipogenesis begins with acetyl CoA and advances by adding two carbon atoms
from another acetyl CoA. This process is repeated until the appropriate length
of fatty acids is obtained. Because this is a bond-creating anabolic activity, ATP
is utilized. Triglycerides and lipids, on the other hand, are a good way to store
the energy that carbs provide. Triglycerides and lipids are high-energy
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molecules that are stored in adipose tissue until they are needed. In conclusion,
acetyl CoA accumulation positively impact the cascade of ATP production,
ketogenesis and lipogenesis.

3. For each case, identify what pathway(s) is/are involved and describe how the
processes in that pathway(s) contribute to the illness/ metabolic disorder or its
recovery. [20M]

i) “The anti-diabetic activity of Moringa oleifera has been reported in several

studies in sub-Saharan Africa and in other parts of the world. Leaves
of M.oleifera are suitable source of green leafy vegetables to reduce diabetic
complications in diabetic patients. Aqueous extract inhibits the activity of α
amylase and α glucosidase; it improves antioxidant capacity, glucose
tolerance and rate of glucose uptake in yeast cell.” [5M]

Hydrolysis in carbohydrate metabolism

Carbohydrate digestion is mediated by the enzymes alpha glucosidase and

alpha amylase. By catalysing the hydrolysis of α-1,4-glycosidic bonds, α-
amylase breaks down alpha-linked polysaccharides like starch and glycogen
into dextrin and maltose. The non-reducing end of the polysaccharide's α-
1,4-glycosidic bond is then hydrolysed by α-glucosidase, which transforms
it to glucose. The aqueous extract of Moringa oleifera inhibits α-amylase and
α-glucosidase, limiting carbohydrate breakdown and lowering carbohydrate
hydrolysis and absorption in the GI diet. This is due to the presence of
natural α-glucosidase inhibitors in M. oleifera extract, such as terpenes,
alkaloids, and flavonoids. Aqueous M. oleifera extract suppresses
carbohydrate digestion, delays glucose uptake, and reduces blood sugar
levels by inhibiting alpha-glucosidase and alpha-amylase enzymes. As a
result, M. oleifera extract has the potential to lower post-prandial blood
glucose levels, making it an effective strategy for regulating blood glucose
levels in type 2 diabetics.

ii) “Fructose 1,6-biphosphatase deficiency is associated with an impaired ability

to form glucose from other substrates. Symptoms include severe
hypoglycaemia, intolerance to fasting, and enlargement of the liver. Rapid
treatment of hypoglycaemic episodes with intravenous fluids containing
glucose and the avoidance of fasting are the mainstays of therapy. Some
patients require continuous overnight drip feeds or a bedtime dose of corn
starch in order to control their tendency to develop hypoglycaemia”. [5M]

Gluconeogenesis

The metabolic process by which organisms produce sugars from non-

carbohydrate substrates for catabolic processes is known as gluconeogenesis.
Fructose 1,6-bisphosphatase (FBPase) is an important enzyme in
gluconeogenesis. FBPase catalyses the conversion of fructose 1,6-bisphosphate
to fructose 6-phosphate. It's one of three gluconeogenesis reactions that aren't
exactly the same as their glycolysis counterparts. Dephosphorylation of fructose
6-phosphate in gluconeogenesis produces no ATP, but phosphorylation of
fructose 6-phosphate in glycolysis does. A metabolic inborn defect characterised
by an enzyme block during the last stages of gluconeogenesis is known as
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FBPase deficiency. FBPase deficiencies prevent lactic acid, amino acids, pyruvic
acid, and glycerol from being converted to glucose, causing hypoglycaemia and
the build-up of gluconeogenic substrates. Patients with FBPase deficiency
appear symptomatic with severe hypoglycaemia, metabolic acidosis, increased
liver enzymes, and lactic acidosis after exposure to risk factors such as long-
term fasting, infection or a high fructose load. As a result, to maintain
normoglycaemia, patients with FBPase deficiency must rely on glucose intake
and glycogen breakdown.

iii) “If enzymes responsible for glycogen degradation are blocked so that
glycogen remains in the liver or muscle, a number of conditions known as
glycogen storage disorders (GSD) can arise. Depending upon which enzyme
is affected, these conditions may affect the liver, muscles, or both. In GSD
type I, the last step in glucose release from the liver is defective, leading to
hypoglycaemia”. [5M]

Glycogenolyis

Glycogenolysis is the breakdown of glycogen into glucose-1-phosphate and

glycogen. The phosphorylase kinase and glycogen phosphorylase enzymes
are in charge of controlling the process. However, in this case, the enzyme
involved is glucose-6-phosphatase (G6Pase), which is found in the liver and
kidney, responsible for the synthesis of glucose for release into the
bloodstream. G6Pase catalyses the terminal step of glycogenolysis and
gluconeogenesis in the liver. G6PC and SLC37A4 gene mutations hinder
effective glucose 6-phosphate (G6P) breakdown. These mutations induce
enzyme deficiencies in the affected organs, preventing glycogen
degradation, resulting in an excess of glycogen and fat in the tissues, as
well as low blood glucose levels. As a result of the inability to hydrolyse G6P
into glucose and inorganic phosphate, G6Pase insufficiency (also known as
Von Gierke's illness) causes severe hypoglycaemia. In conclusion, G6Pase
deficiency leads to insufficient glycogen breakdown, resulting in low blood
glucose levels and thus, hypoglycaemia.

iv) “Some fatty acid oxidation disorders arise through dysfunction of carnitine
transport enzymes, although most of these conditions are caused by fat-
degrading enzymes directly involved in the beta-oxidation cycle itself.
Treatment with carnitine is partially effective. Fatty acid oxidation disorders
are commonly manifest with hypoglycaemia, liver disease, decreased
muscle tone, and heart failure”. [5M]

Fatty acid β-oxidation

Two common diseases linked to beta oxidation of fatty acids are carnitine
uptake defect and carnitine palmitoyltransferase II deficiency. This is linked
to abnormalities in fatty acid transport into mitochondria and oxidation
defects, which can lead to reduced energy output from fatty acid oxidation.
The carnitine shuttle is a mechanism that transports long-chain fatty acids
into the mitochondrial matrix for β-oxidation, a process in which fatty acids
are oxidised in the mitochondrial matrix for energy production. Carnitine
acyltransferases are involved in the carnitine shuttle. Carnitine
acyltransferase mutations cause hypoketonemia and hypoglycaemia,
while carnitine palmitoyltransferase II deficiency is the usual factor of
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abnormal lipid metabolism in skeletal muscle. In fatty acid oxidation

disorders, hypoglycaemia is induced by a decrease in hepatic glucose output
and an increase in peripheral glucose uptake. In certain conditions, dietary
supplementation with carnitine has been proven to help alleviate symptoms.

(PLO3, C4)

- End of question paper –

- Kertas soalan tamat -

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