IASM: Cell metabolism

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1. What is the suc = glu + fru 12. Fasting state fuel has to be provided without
difference depletion of blood glucose (affect
between malt = glu + glu anerobic respiration + water
sucrose, maltose, potential)
lactose, starch sta = n(malt)
13. Mechanism of takes place in the cytoplasm, where
and glycogen?
phosphorylation of glucose is converted into glucose-
gly = n(glu)
glucose 6-phosphate and ADP using ATP
2. How are 1) Long-chained carbohydrates under enzyme hexokinase
carbohydrates hydrolyzed by salivary α-amylase to form
14. Why does to ensure glucose stays in the cell
digested? α-dextrins;
phosphorylation and is not recognised by
occur? transporter
2) Dextrins further hydrolyzed by
pancreatic α-amylase to form tri and 15. What pathways are glycolysis, gluconeogenesis,
oligosaccharides and maltose etc.; G6P involved in? glycogen synthesis and pentose
phosphate pathway
3) Disaccharides broken down into 16. Name the enzyme hexokinase, in cytoplasm
monosaccharides by maltase, isomaltase, required and location
sucrase and lactase on intestinal wall; for phosphorylation of
glucose into G6P
4) Monosaccharides absorbed by
17. How is galactose and galactose drive synthesis of
intestinal wall.
fructose involved in glycogen and provides energey,
3. Name 2 soluble (.˙. kept in insoluble form of gly) + glucose metabolic while fructose only provides energy
properties of needs to be transported by facilitated pathway?
glucose diffusion and is Na+ dependent)
18. Describe the process ...
4. Glycolysis conversion of glucose into pyruvate (in of glycolysis
cytosol)
19. Describe the process oxaloacetate (4C) + acetyl CoA →
5. Function of Provides metabolic energy + precursor of TCA cycle
glycolysis molecules for synthesis (eg AAs) (OCIKSSFM) citrate (6C) →
6. Gluconeogenesis generation of glucose from non-CHO
substrates (eg pyruvate, glucogenic AAs, isocitrate →
glycerol etc)
alpha-ketaglutarate (5C) →
7. Function and Maintains constant supply of glucose (esp
location of in fasting state) + mainly in liver
succinyl CoA (4C) →
gluconeogenesis
8. Glycogenesis synthesis of glycogen from glucose succinate (4C) →
9. Function and Produces glucose from glycogen (in
fumerate (4C) →
location of times of starvation, physical exercise and
glycogenesis stress) + muscle and liver
malate (4C) →
10. Glycogenolysis breakdown of glycogen stored in the liver
into glycose oxalocetate
11. What triggers decrease in level of insulin and increase 20. Describe the process ...
the processes of in level of glucagon which causes the of oxidative
gluconeogenesis break down of muscle and fat cells in phosphorylation
and amino acids and glycerol respectively for
glycogenolysis? the synthesis of glucose in the liver.

Along with glycogen stored in the liver,

both are converted into soluble forms to
enter the bloodstream.
21. Name the four generation of cellular energy 29. Why do cells use ATP the energy required to break the
functions of glucose produced from phosphate bonds in fuel
metabolism precursor of fat synthesis metabolism of fuel molecules is greater than the
molecules (e.g. energy required to convert ADP
precursor of amino acid synthesis carbohydrates, protein, to ATP
fats) .˙. hydrolysis of P bonds can be
conversion to storage and complex coupled with the formation of
carbohydrates ATP
22. What are the three glycolysis 30. Name and describe the substrate-level phosphorylation
processes involved in pathway of anaerobic
generation of TCA cycle generation of ATP in e.g. hydrolysis of 1,3-
cellular energy? glycolytic pathway biophosphoglycerate at
oxidative phosphorylation phosphoglycerate kinase
23. What are the three glucose → serine → cysteine +
e.g. hydrolysis of
pathways for amino glycine
phsophoenolpyruvate at
acid synthesis?
pyruvate kinase
pyruvate → alanine
31. Name 3 electron rotenone, cynaide, carbon
TCA cycle → glutamate and other transport inhibitors of the monoxide
a.a. oxidative phosphorylation
24. What are the three Glu → Gly3P → Glycerol 32. Name an uncoupling 2,4-dinitrophenol
pathways for fat agent inhibitor of the
synthesis synthesis? Glu → Pyruvate → Acetyl CoA → oxidative phosphorylation
FA
33. Name an ATP synthase oligomycin
CoA →FA
inhibitor of the oxidative
phosphorylation
Glycerol + FA → TG
34. How does an uncoupling uncoupling agent dissipates the
25. What are two glucose → G6P → G1P → UDP-gluc
agent function to stop proton gradient by opening
pathways for → glycogen
generation of ATP? channels for protons to move
conversion to
out of the inter-membranous
storage and complex UDP-gluc → glycoproteins,
space.
carbohydrates? glycolipids, proteoglycans,
glucronides 35. If ΔG of substrates is ATP synthesis by substrate-level
lower than ΔG of ATP, phosphorylation
26. Describe glucogenic a.a. → Acetyl-CoA →
what occurs?
gluconeogenesis as a pyruvate → gluconeogensis
pathway for net 36. If ΔG of substrates is synthesis of substrates is
synthesis of glucose TG → lipolysis → FA → beta- higher than ΔG of ATP, powered by ATP hydrolysis
oxidation → Acetyl-CoA → pyruvate what occurs?
→ gluconeogensis 37. Name the two enzymes phosphofructokinase (PFK)
27. Why is ATP preferred ATP hydrolysis is thermodynamically that regulate glycolysis
as the "biological favourable, and when coupled with pyruvate kinase (PK)
currency of energy?" endergonic reactions, drive the 38. What is the difference PFK-1 converts Fructose-6-P to
reaction between the PFK-1 and Fructose-1, 6-P2
28. Fuel-molecule A molecule metabolised by a cell to PFK-2?
generate adenosine triphosphate PFK-2 converts Fructose-6-P to
(ATP) and NADPH .˙. generally have Fructose-2, 6-P2
high-energy phosphate bonds 39. What molecule is a ATP binds to the allosteric site
negative allosteric of the enzyme PFK-1, thereby
regulator of PFK-1? limiting Fructose-6-P at high
[ATP]
40. What molecules is F-2,6-P2 (product of PFK-2) stimulates 51. How are amino acids amino acids → acetyl Co-A → ATP
a positive PFK1 production which converts F-6-P involved in ATP released in TCA cycle
allosteric Fructose-1, 6-P2 production?
regulators of
52. How is at low oxaloacetate concentrations,
PFK-1?
gluconeogenesis less than acetyl-CoA enters the TCA
41. How does insulin insulin stimulates the removal of regulated by cycle and is convered to
and glucagon phosphate to form PFK-2 → F-2, 6-P2 → oxaloacetate? acetoacetyl-CoA and ketone bodies
regulate PFK-2? PK1 → F-1, 6-P2
53. Name 3 N-containing glutathione, creatine phosphate,
compounds that use monoamine neutransmitters
glucagon inhibits PFK-2 by forming
amino acids as
phosphorylated PFK-2.
precursors
42. Which molecule is F-1, 6-P2
54. Name 2 purine Purine = adenine, guanine
a positive
nucloetides (PURe as
allosteric
AG)
regulator for PK?
55. Name 2 pyrimidine Pyramidine: cytosine, uracil, thymine
43. Which molecules ATP, Alanine
nucleotides (CUT the
are negative
PY)
allosteric
regulators for 56. What is the Nucleotide = sugar + base +
PK? difference between phosphate
the structure of
44. What are the glucose → G6P → G1P → glycogen
nucleotides and Nucleoside = sugar + base
substrates and
nucleosides
products of
glycolysis? 57. Why are nucloetides e.g. ATP, ADP, AMP
needed for metabolic
45. What are the pyruvate → oxaloacetate (via pyruvate
functions of cells? Conversion of high energy form
substrates and caboxylase) → phosphenolpyruvate →
(Give examples) (ATP) to low energy (AMP) releases
products of F-1, 6-P2 → F-6-P → G-6-P → glucose
energy in cell
gluconeognesis
46. X How is blood Glucagon stimulated → phosphorylated Greater no. of phosphates
glucose lowered PK2 → decrease F-2, 6-P2 → inactivates
58. How do nucloetides Adenosine receptors are found in
via glycolytic rate PFK1 → lowers glycolytic rate → stop
act as hormone-like many cells e.g. neutrophils,
after a meal? use of glucose into pyruvate → higher
molecules? (Give macrophages
glucose concentration
examples)
47. How is blood Insulin stimulated → removal of
59. How do nucleotides GTP control duration of activity of
glucose phosphate from PK2 → increase in F-1,
act as molecular enzyme/molecule
decreased via 6-P2 → increases glycolytic rate →
times?
glycolytic rate at converts glucose to pyruvate → lower
Molecules/enzymes has to be
fed state? glucose concentration
activated intermittently for reaction
48. How are amino During transcription, amino acids are to go on
acids converted arranged by t-RNA into polypeptides
into proteins? that form proteins depending on how GTP binds to G-proteins (active) →
they are structured hydrolyzed → GDP binds to G-
proteins (inactive)
49. How are amino glucogenic amino acids → acetyl Co-A
acids involved in → pyruvate → glucose 60. Describe the pathway Nuceloside triphosphate (NTP)
gluconeogenesis? for synthesis of converted via RNA polymerase into
ribonucleic acids RNA
50. How are amino ketogenic amino acids → acetyl Co-A
acids involved in → ketone bodies 61. Describe the pathway Deoxyribonucleoside triphosphates
ketogenesis in for synthesis of (dNTP) converted via DNA
the liver? deoxyribonucleicside polymerase into DNA
triphosphates
62. How are nucleotide From nucleoside diphosphates 68. What are the 4 Triacylglycerol (TAG)
triphosphates and (NDP) and deoxyriboncleoside main forms of
deoxynucleotide diphosphates (dNDP) using ATP lipids? Cholesterol (Ch_
triphosphates formed?
Phospholipid
63. Why is the "salvaging de novo synthesis is metabolically
pathway" preferred costly (energy and materials)
Glycolipid
over de novo
synthesis for "salvaging pathway" uses existing 69. Classify lipids Storage (neutral) = TAG in adipose tissue
additional supply of purine and pyrimidine bases into eiher storage
nucleotides (important for brain cells) lipids or Membrane (polar) = phospholipids,
membrane lipids glycolipids
64. Cause and symptoms Defect in salvaging pathway:
of Lesch Nyhan purine bases cannot be recycled 70. Name 3 Low solubility in water
syndrome (salvaging properties of
pathway) Brain cells cannot perform de novo lipids Relatively hydrophobic nature (polar
synthesis heads)

Continuous loss of purine bases in Distinctive alkyl groups

uric acid formation
71. Give definition Chemical compound with both
and examples of hydrophilic and hydrophobic properties
Impaired brain development
amphiphiles
65. Cause and symptoms Purine nucleotides with removal of Phospholipids: polar head with two non-
of Gout (de novo) phosphate, forms purine polar tails
nucleosides
Fatty acid salts: polar head and non-
Purine nucleosides forms xanthine polar tails
with removal of ribose
Bile acid/salts: emulsifies oils by its
Another precursor of uric acid is amphiphilic properties
guanosine
Cholesterol: 4 hydrophobic carbon rings
Under xanthine oxidase, uric acid is with hydrophilic OH group
formed
72. How does β- 1) Hormone-sensitive lipase mobilises fat
oxidation allow from adipose tissues
Inefficient uric acid excretion
for energy
results in accumulation, leading to
usage? 2) Fatty acids exit adipocytes, and are
formation of crystals at joints
carried by serum albumin in the blood
66. How can nucleotide Basic: enzyme inactivators inhibits stream and carried to tissues in high
metabolism deoxynucleotide production → no demand for energy
mechanisms treat DNA → stops proliferation of
cancer? cancer cells 3) Fatty acids are escorted into
mitochondria where β-oxidation takes
e.g. 5-fluorouracil affects dTTP place in the matrix
67. How can nucleotide Basic: devise compound that
4) β-oxidation consists of repeated
metabolism inhibits xanthine oxidase → inhibits
removals of acetyl groups to acetyl CoA
mechanisms treat production of uric acid → prevents
until ATP is formed
gout? accumulation of uric acid crystals
at joints → prevents gout
*5ATP is released each cycle from 1
NADH and 1 FADH
73. Name 5 Chylomicrons, VDL, 77. How and where are Muscle: FA → CO2 + H2O
lipoproteins that IDL, fatty acids broken
transport lipids in LDL, down/digested? Adipose tissue: FA → FA CoA →
order of protein- HDL G6P → glycerol 3P → FA CoA +
to-lipid ratio glycerol 3P → TAG storage
74. Describe the 4 rigid carbon rings intercalated in a 78. How and where are Liver: via transporters on liver cell
structure, synthesis monolayer of chylomicrons to provide glycerols broken surface
and functions of rigidity down/digested?
cholesterol
79. How and where are Liver:
Synthesized from acetate and acetyl
chylomicron remnants
CoA in liver
broken down/digested? Apoprotein E binds to receptors
for endocytosis into cell
Involved in producing bile salt, steroid
hormones, blood lipoproteins and
Digested by enzymes of
membrane
lysosome in endocytic vesicles in
liver cells
Cholesterol readily enters cell
membrane (compared with bile salt w/ 80. Describe the 1) Synthesis of TAG from glucose
hooked shape) production of in liver:
triacylglycerol Glucose → Glycerol 3P →
75. Describe the 1) Emulsification of bile salts to form
Glycerol 3P + FA CoA → TAG
packaging of micelles (hydrophilic monolayer)
triacylglycerol into
2) Packaging of TAG into VLDL in
chylomicrons 2) Digestion by pancreatic lipase on
liver with B-100 apoprotein,
surface of bile-salt-TAG structure into
cholesterol and phospholipids
FA and 2-monoacylglycerol
3) Exocytosis of VLDL into
3) Transcellular absorption in nascent
bloodstream and exported to
chylomicrons (lacking apoproteins)
peripheral tissues for usage and
storage
4) FA and 2-monoacylglycerol enters
from intestinal lumen by diffusion into
4) VLDL digested by lipoprotein
enterocytes
lipase under apo Cii → FA +
glycerol
5) FA and 2-monoacylglycerol
undergo re-esterification in sER into
5) VLDL converted into IDL, then
TAG
to LDL

6) Along with B-48 apoprotein
synthesized in rER, TAG is packaged in
Golgi apparatus into chylomicrons
76. Describe the 1) Chylomicrons with TAG secreted by
transport and exocytosis from cell
digestion of
chylomicrons 2) Chylomicron carried in lymph to
blood cappillaries (prevents fat
globules from forming plaques in
arteries)
3) Digested in FA, glycerol and
chylomicron remnants by lipoprotein
lipase (LPL) on blood capillary wall
under presence of apolipoprotein Cii
81. What are plant sterols? Steroid compounds similar to
cholesterol which occur in plants
82. Absorption of dietary 1) Absorption of dietary
cholesterol and plant cholesterols and plant sterols in
sterols the jejunum of small intestine
2) NPC1L1 selectively absorbs
dietary cholesterol from micelles
in the lumen of the small intestine
3) Endosomal sorting: subapical
endomes cross a sorting
compartment
83. Effects of uptake 1) Supplied to cell membrane or 88. Name a disease that occurs Athersclerosis
of LDL-cholesterol production of steroid hormones when reverse cholesterol
transport
2) Repressive synthesis of HMG-CoQ
89. Name two rate limiting steps Reduction of HMG-CoA
reductase to lower cholesterol
in cholesterol synthesis in
productivity
the liver Statins

3) Stimulate storage of cholesterol as 90. What is the Cori cycle? Under anaerobic conditions,
ester the contracting muscle
produces lactate instead of
4) Repress synthesis of LDL receptor pyruvate
which prevents over-uptake by cells
but accumulates in bloodstream Glyconeogenesis in the liver
converts lactate into
84. Describe the 1) HDL is generated by the small
pyruvate and glucose
synthesis of HDL intestine and liver through the secretion
of lipid-free apoA-I 91. How does glucose Glycogen in liver is
metabolism release glucose converted in glucose via
2) ApoA-I then recruits cholesterol during less intense but calcium ions and cyclic AMP
from these organs through the actions prolonged exercise? (epinephrine), and then
of the transporter ABCA1, forming transported to muscle
nascent HDLs 92. How does amino acid and Via the glucose-alanine
85. Describe the 1) Nascent HDL collects free glucose metabolism cycle between the liver (glu)
pathway for cholesterol from tissue cells incl. integrate during less intense and skeletal muscle (alanine)
reverse cholesterol macrophages from ABCA1 but prolonged exercise?
transport through 93. How are fatty acids in the Activated TAG lipase
HDL 2) The unesterfied cholesterol in adipose tissue converted for converts TAG into
nascent HDLs is esterified to use in muscle during less diacylglycerol, which
cholesteryl ester by the enzyme LCAT intense but prolonged produces free fatty acids via
(mature HDLs) exercise? glycerol
94. What is VLDL and its VLDL( Very low density
3) Mature HDL collects free
function? lipoprotein): carry
cholesterol from macrophages through
triglycerides from the liver to
ABCG1
cells for energy as needed
86. Describe the direct HDL interacts with receptor SR-B1 in or stored as fat.
pathway for the liver and discards cholesterol
95. What is LDL and its LDL (low density
cholesterol to
function? lipoprotein): rich in
return to the liver HDL is then recirculated
cholesterol
87. Describe the 1) Cholesterol is transported through
indirect pathway cholestryl ester transport protein Delivers cholesterol to
for cholesterol (CETP) to VLDL and LDL peripheral cells after
triglycerides deposited.
2) CETP transports TAG to the HDL
96. What is HDL and its HDL (High density
function? lipoprotein): gathers up extra
3) PLTP (phospholipid transport
cholesterol to transport back
protein) transports phospholipids to
to the liver.
HDL
97. What is chylomicron and its Large lipoprotein mainly
4) Cholestrol-rich VLDL and LDL function? composed of TAG
interacts with receptors in liver and are
digested by lysosome action → bile Responsible for transporting
salts → cholesterol excreted dietary triglycerides and
some cholesterol (in fasting
state)
98. What is produced Guanine triphosphate 107. How does 1) ATP is a negative allosteric regulator of
during substrate- allosteric PK1, an enzyme that controls the
level regulation glycolytic pathway
phosphorylation? modify enzyme
catalysis? AMP (positive) reverses the inhibitory
99. Which of the AMP
action of ATP, and so the activity of PK1
metabolites can
and glycolysis increases when energy
increase the pace of
charge
glycolysis in
skeletal muscle
This occurs when AMP accumulates in the
during high intensity
muscle
exercise?
100. What is the Stimulation of glycolysis and 2) Release of calcium ions (positive) into
regulatory effect of inhibition of gluconeogenesis via muscle during nerve impulse stimulates
Fructose-2,6- regulation of insulin and glucagon glycolysis
bisphosphate?
101. Which chemical Glycogenesis and glycogenolysis G6P (negative) inhibits glycolysis
relationships are 108. What is the ATP derivative
reciprocals in the FA synthesis and FA breakdown substrate of
liver and 1) muscle adenylyl cAMP is a secondary messenger that
and 2) adipose cyclase in the regulates its target proteins
tissue synthesis of
102. What processes are 1) Liver and muscle: glycogenesis cAMP?
stimulated in fed 109. Which of the Palmitate
state? 2) Liver and adipose tissue: FA following is a
synthesis non-
103. What processes are 1) Liver and muscle: glycogenolysis carbohydrate
inhibited in fed derivative from
state? 2) Liver and adipose tissue: FA glucose
breakdown by LPL into mitochondria metabolism?
for oxidation 110. What does Apoenzyme = inactive form
apoenzyme Holoenzyme = activated form due to
3) Muscle: protein breakdown and attachment to co-enzyme
104. How are ketone For general energy consumption holoenzyme
bodies involved in during fasting state, espc in brain mean?
ketogenesis 111. Name two B vitamin (organic)
metabolism in Ketone bodies are produced from types of Fe, Cu (inorganic metal ions)
starvation? acetyl-CoA in the mitochondrial coenzymes
matrix of liver cells when and give
carbohydrates are so scarce, energy examples of
must be obtained from breaking each
down fatty acids
112. Differentiate Oligo = one enzyme bind to several
105. What fuels are used Muscle ATP, phosphocreatine, between substrate molecules
during heavy bursts glycogen oligomeric and Mono = one enzyme, one substrate
of activity? monoeric
106. What fuels are used Muscle ATP, phosphocreatine, enzyme
during moderate Glycogen (oxidative 113. What are Protein Kinases are enzymes that modify
bursts of activity? phosphorylation) protein kinases the function of other proteins by attaching
are and give phosphate groups to them, involved in
examples of its many pathways incl. ADP conversion to
significance ATP by PK, cyclin-dependent kinase for
cell division control
114. Name two Vitamin A and D 124. What does a cream layer Increased chylomicrons and
vitamins that use and infranatant rabid to VLDLs
lipids as hormone opaque appearance of
precursors serum in standing plasma
test suggest?
115. What is the Blood clot formation
significance of 125. Describe the endogenous 1. TAG synthesis in liver
vitamin K as a pathways of lipid packaged into nascent VLDL
cofactors for metabolism w/ ApoB-100
enzymes
2. ApoC-II and ApoE transfer
116. Describe the Steroid nucleus of four fused rings
from HDL to VLDL
structure of Hydroxyl group (polar head) attached
sterol to A ring
3. Lipoprotein lipase
Alkyl side chain
activated by ApoC-II,
117. Describe the Begins with C14 and removes one acetyl degrades TAG in VLDL
simplified beta moiety in form of acetyl CoA
oxidation 4. IDLs's ApoC-II and ApoE
pathway e.g. C14 - C12 - until C4 returned to HDL
118. What is the role ApoC-II activates lipoprotein lipids to
of ApoC-II in allow release of FFA 5. LDLs w/ greater CE p than
lipid transport? TAG binds to specific
receptors aided by heparin
119. How is VLDL Cholesteryl starts and TAGs from excess
sulfate on hepatocyte of
formed? FA and cholesterol form VLDL with
liver
ApoB-100 in the liver
126. Describe the exogenous 1. Bile salts form micelles
120. Describe the fate Removal of TAG from VLDL produces
pathway of lipid metabolism around ingested fats and oils
of VLDL LDL which collects cholesterol and
cholesteryl esters and carries it from
2. Micelles absorbed in
liver to muscle and adipose tissue
small intestine by GI
121. Describe the 1. Carry cholesterol from liver to muscle lymphatic system
function of LDLs and adipose tissue
2. LDL receptors recognise apoB-100 3. Nascent CMs w/ ApoB-48
and enables myocytes and adipocytes collect ApoC-II and ApoE
to take up cholesterol from HDL
122. Describe the Carries out reverse cholesterol transport
function of HDLs - contains a lot of protein e.g. ApoA-I, 4. Enter blood plasma and
ApoC-II, ApoE extra cellular lipoprotein
- picks up cholesterol from cells and lipase is activated by ApoC-
returns them to liver II and FFA to adipose,
glycerol to liver
123. What is LCAT and Lecithin-cholesterol acts transferase
describe its - catalyse the formation of cholesteryl 5. ApoC-II returned to HDL
function Ester from lecithin and cholesterol so that only CM remnant
- converts cholesterol of CM and VLDL remains
remnants to cholesteryl esters
6. CE-rich CMr binds it's
ApoE to specific receptor on
liver and are endocytosed
127. Describe how HDL is 1. Excess cholesterol in 134. Describe how high levels 1. Small size of LDL infiltrates
formed peripheral cells binds to free of LDL can cause activated endothelium by
apoA-I extracellularly atheroma passive diffusion

2. Nascent HDL develops into 2. Causes degeneration of

mature HDL by LCAT (transferase artery walls by accumulation of
enzyme) with internalised fatty deposits (atheroma)
cholesteryl ester
135. Describe how endothelial Increased permeability,
can be activated by increased inflammatory
3. Transfer of cholesterol to
inflammation cytokines, decreased
VLDL, IDL, LDL for transport to
vasodilation and anti thrombotic
liver
molecules
128. How does - affects exogenous pathway
136. Describe how arterial Increased inflammatory
chylomironaemia affect - defective ApoC-II prevents
smooth muscle cells can cytokines, extracellular matrix
normal lipid TAG breakdown by LPL
be activated by synthesis, and migration into
metabolism? - no FFA to adipose tissue, no
inflammation intima and proliferation
glycerol return to liver
137. How is atherscleortic 1. Accumulation of lipoprotein
129. How does familiar - affects endogenous pathways
lesion formed? particles in intima
hypercholesterolaemia
affect normal lipid Type IIa
2. Induces local cytokines
metabolism - defective LDL receptor on liver
elaboration and leukocyte
prevents uptake of LDL at end of
migration into intima
endogenous pathway
- increases circulation of LDLs
3. Leukocytes e.g. monocytes
develop into foam cells
Type IIb
- Also defective ApoB-100
4. Smooth Muscle Cells migrate
results in increase in circulating
into intima from media
VLDL, LDL, IDL
130. How does - affects both endo and exo 7. Extracellular matrix promotes
dysbetalipoproteinaemia pathways matrix accumulation and fatty
affect normal lipid - defective ApoE prevents streak
metabolism binding of LDL and CMr to liver
8. Lesion, and calcification
131. Name the two diseases Familial hypercholesterolaemia
occurs, resulting an acellular
that causes type IIa and type IIb
fibrous capsule surround a lipid
hypercholesterolaemia
rich core (granuloma)
(Defective LDL and ApoB-100 In
endogenous pathways prevents 138. Describe the progression Fatty streak - endothelial
uptake of LDL (C>TAG) to liver) from fatty streak to dysfunction, leukocyte
plaque progression to recruitment, foam cell for,action
132. Name a disease that Sporadic hypertriglyceridemia
plaque disruption
causes
Plaque progression - SmMCs
hypertriglyceridemia (Results in low LPL which
migration, lipid core formation
prevents TAG breakdown in
muscles and adipose tissue)
Plaque disruption - thrombus
133. Name the gene that PCSK9 formation
regulated the expression
139. Name three molecules of Bile salts
of LDL receptors (Important as LDL is cholesterol
which cholesterol is a Vitamin D
rich and its circulation can lead
precursor Steroid hormones
to atheroma)
140. What is the function of Receptors that absorbs free
Neimann-pick C1-like 1 cholesterol in bile acid micelle
NPC1L1 into intestine (enterocytes)
141. What is the function of
acetyl coA acetyl
transferase ACAT2?
142. Name two types of gut
bacteria that facilitates the
production of secondary
bile acids
143. Name a factor that
reduces bile acid excretion
and thus cholesterol
utilisation
144. Briefly describe the
process of cholesterol
synthesis
145. Name the enzyme that
controls cholesterol
synthesis
146. Name a type of regulation
that favour upregulation of
expression for gene for
HMG CoA reductase
147. Name a symptom that is
caused by both
heterozygous and
homozygous familial
hypercholesterolaemia
148. Describe a phenotypical
abnormality related to fat
metabolism that can be
detected with standing
plasma test
Free cholesterol inside
enterocyte (cell of intestines)
converts to CE by ACAT2
Lactobacillus and
bifidobacterium makes
secondary bile acids which
helps excretion of primary bile
salts and cholesterol utilisation
Age (results in rise in
cholesterol due to decreased
demand for bile acid
synthesis)
1. Conversion of acetyl CoA to
mavalonic acid
2. Use of ATP to form
activated isoprene
3. Formation of squalene from
isoprene
4. Cyclisation to convert
squalene to cholesterol
HMG CoA reductase
Increase in insulin and
thyroxine = Increase in
cholesterol
(Glucagon and
glucocorticoids have opposite
effect)
Xanthomas - irregular yellow
patch or nodule on the skin,
caused by deposition of lipids
Normal: serum, jelly red cells
after centrifuge of blood and
jelly
Lipaemia: plasma (serum) is
white yellowish and cloudy
149. How is sugar metabolised
into fat?
150. Name an intermediate
product of TCA produced by
the breakdown of glutamine
that can be used as a source
of new C in gluconeogenesis
151. Name two non-glucose
products used as a fuel in
fasting state
152. Describe how glutamine is
metabolised in kidney cells
in fasting state for
gluconeogenesis
153. Define one-carbon
metabolism
1. High blood glucose
levels triggers the release
of insulin from pancreatic
beta cells
2. Stimulates the uptake of
glucose into hepatocytes
and adipose tissue
3. Hepatic glycolysis
(stimulated by insulin)
converts glucose into
pyruvate, then to acetyl
CoA
4. Excess acetyl CoA is
channeled into fatty acid
synthesis for the production
of increased TAG
5. TAG synthesised in the
liver is packaged into VLDL
for secretion into the
bloodstream and taken up
by adipose tissue for
storage as fat
alpha-ketoglutarate
glutamine → ammonium +
a-ketoglutarate (via
glutamate dehydrogenase)
→ TCA → OAA →
gluconeogenesis
Glutamine (kidney)
Ketone bodies (liver)
Glutamine → glutamate
(glutaminase) → a-
ketoglutarate → TCA (w/
ACoA*) → OAA → CO2 →
gluconeogenesis
*FA → beta-ox → ACoA
*Pyruvate → ACoA
Amino acid metabolism that
requires the transfer of one
carbon at a time due to one
carbon group's volatility
154. Name the three major 1. Tetrahydrofolate (THF) = 160. Name the alternative rule molecule used in Glucose
groups of atoms required cofactor in enzymatic early ischaemia for generation of ATP
in one-carbon metabolism reactions

2. Vitamin B12 (Cobalamin) =

coenzyme in methylation +
rearrangement reactions

3. S-adenosylmethionine
(SAM) = methyl donor
155. How is tetrahydrofolate Diet = ingestion of vitamin folic
acquired in our bodies? acid in "leafy greens"

Use of dihydrofolate reductase

to reduce into tetrahydrofolate

Made of PABA and glutamic

acid
156. Name the carbon groups ...
that can be carried by
tetrahydrofolate in one
carbon metabolism
157. Name the preferred fuel Fatty acid
molecule for ATP
generation in
cardiomyocytes under
aerobic conditions
158. During high intensity Stored ATP
exercise, muscle relies on Creatinine phosphate
which three fuels for Anaerobic glycolysis of
energy muscle glycogen (into lactate)
159. Name the preferred rules Oxidation of fatty acid via
used in prolonged breakdown of fat in adipose
exercise and its pathway tissue (lipolysis)
to produce ATP
*low blood sugar = high
glucagon = mobilise fatty
acids from adipose = beta
oxidation = acetyl CoA

Excess acetyl coA = decreased

activity of pyruvate
dehydrogenase to block
conversion of pyruvate into
acetyl CoA

FA oxidation inhibits glucose

entering citric acid cycle and
oxidative phosphorylation