BIOCHEMISTRY 2nd Session

BIOCHEMIST
RY
Review
Jan Reynald Shane A. Coquilla, MD, MPH
February 21
2023
OUTLINE
Quick Review on Biochemistry
Simulated Preboard Questions and
Review on Basic Concepts
• NUCLEOTIDES
• NUCLEOTIDE METABOLISM
• LIPIDS
• LIPID METABOLISM
• CHOLESTEROL
• BILE SALTS
• LIPOPROTEIN
ADD A FOOTER 2
QUESTION
6. Which of the following components are found in DNA

A. A phosphate group, guanine, and deoxyribose
B. Thymine and deoxyribose
C. A phosphate group, adenine and ribose
D. Cytosine and ribose
ADD A FOOTER 3
QUESTION
6. Which of the following components are found in DNA

A. A phosphate group, guanine, and deoxyribose
B. Thymine and deoxyribose
C. A phosphate group, adenine and ribose
D. Cytosine and ribose
ADD A FOOTER 4
NITROGENOUS BASES
• Nitrogen-containing heterocycles
• Purine & Pyrimidine
NITROGENOUS BASES
• The smaller pyrimidine

molecule has the longer
name
• The larger purine molecule
has the shorter name
• Rings – numbered in the
opposite direction
NUCLEOSIDES
• Derivatives of purines and

pyrimidines
• With SUGAR
• Numbers with prime –
distinguish atoms of sugar
from those in the
heterocycle (2’, 3’, 5’…)
NUCLEOSIDES
• RIBONUCLEOSIDE
• D-ribose
• DEOXYRIBONUCLEOSIDE
• 2-deoxy-D-ribose
NUCLEOSIDES
CHM060: BIOMOLECULES
NUCLEOTIDE
• Phosphorylated nucleosides
• Nucleoside + phosphate group
• Phosphate groups
• Usually attached to the 5’ hydroxyl group of sugar
• Nucleoside diphosphate/triphosphate
NUCLEOTIDES
•Functions
• Precursors of nucleic acids
• Participate in metabolic functions
• Energy metabolism
• Protein synthesis
• Regulation of enzyme activity
• Signal transduction
NUCLEOTIDE
Universal Electron Carriers
•ATP is a
building block
of these
Coenzyme A and cylic AMP
•CoA
• Krebs Cycle
• Lipid synthesis and
oxidation
•cAMP
• Acts as a 2nd messenger
activating Potein
Kinase A
QUESTION
5. Which one is correct concerning purine and pyrimidine metabolism?
A. Purines degrade to CO2 and water

B. Pyrimidines, when degraded yield uric acid
C. Purines cannot be degraded to generate energy
D. Excess pyrimidine degradation can lead to gout
ADD A FOOTER 16
QUESTION
5. Which one is correct concerning purine and pyrimidine metabolism?
A. Purines degrade to CO2 and water

B. Pyrimidines, when degraded yield uric acid
C. Purines cannot be degraded to generate energy
D. Excess pyrimidine degradation can lead to gout
ADD A FOOTER 17
QUESTION
Mr. C, a 45 year old male patient, consulted for knee joint swelling. It was revealed that he ate a plateful
of bopis during a drinking spree the night before. An impression of an acute attack of gout was then given:
7. Which of the following is the ultimate and unique product of purine nucleotide degradation in man
contributory to the patient’s joint swelling and pain?
A. Hypoxanthine
B. Urea
C. Uric Acid
D. NH4+
E. Allantoin
ADD A FOOTER 18
QUESTION
Mr. C, a 45 year old male patient, consulted for knee joint swelling. It was revealed that he ate a plateful
of bopis during a drinking spree the night before. An impression of an acute attack of gout was then given:
7. Which of the following is the ultimate and unique product of purine nucleotide degradation in man
contributory to the patient’s joint swelling and pain?
A. Hypoxanthine
B. Urea
C. Uric Acid
D. NH4+
E. Allantoin
ADD A FOOTER 19
QUESTION
Mr. C, a 45 year old male patient, consulted for knee joint swelling. It was revealed that he ate a
plateful of bopis during a drinking spree the night before. An impression of an acute attack of gout
was then given:
8. One of the following mechanism of allopurinol usually prescribed for the treatment of patients
with gout:
A. Inhibits PRPP synthase resulting to increased excretion of uric

acid
B. Enhances the action of HGRPTase which breaks down uric acid
C. Overall diminishes the de-novo synthesis of purines
D. Inhibits xanthine oxidase by being as structural analog of
hypoxanthine
ADD A FOOTER 20
QUESTION
Mr. C, a 45 year old male patient, consulted for knee joint swelling. It was revealed that he ate a
plateful of bopis during a drinking spree the night before. An impression of an acute attack of gout
was then given:
8. One of the following mechanism of allopurinol usually prescribed for the treatment of patients
with gout:
A. Inhibits PRPP synthase resulting to increased excretion of uric

acid
B. Enhances the action of HGRPTase which breaks down uric acid
C. Overall diminishes the de-novo synthesis of purines
D. Inhibits xanthine oxidase by being as structural analog of
hypoxanthine
ADD A FOOTER 21
NUCLEOTIDE METABOLISM
• Purine generation
• 2 ways
• De Novo Purine Synthesis
• Salvage Pathway
• SYNTHESIS OF PURINE
NUCLEOTIDES
• The purine base is synthesized
on the ribose moiety.
• 5’ phosphoribosyl-1-
pyrophosphate (PRPP)
• formed in the liver
• An activated pentose
NUCLEOTIDES
• Synthesis of 5’-
phosphoribosylamine
• Committed step in purine
nucleotide biosynthesis
• SYNTHESIS OF PURINE NUCLEOTIDES

• Synthesis of inosine monophosphate (IMP)
• Parent purine nucleotide
• 9 steps in the formation
• Requires ATP
• 2 steps require N-10 formyltetra-hydrofolate
• SYNTHESIS OF PURINE NUCLEOTIDES

• Synthesis of inosine monophosphate (IMP)
• Parent purine nucleotide
• 9 steps in the formation
• Requires ATP
• 2 steps require N-10 formyltetra-hydrofolate
• SYNTHESIS OF
PURINE
NUCLEOTIDES
• IMP to AMP and GMP
• Two step energy
requiring pathway
NUCLEOTIDES
• IMP to AMP and GMP
• Each product, by feedback inhibition.
regulates its own synthesis from the
IMP branch point as well as inhibits
the initial step in the pathway.
• AMP and GMP can be
phosphorylated to the triphosphate
level.
• Synthetic inhibitor of PURINE synthesis

• 6-mercaptopurine and azathioprine
• Inhibit de novo purine synthesis
• Mycophenolate and ribavirin
• Inhibit IMP dehydrogenase
• Structural analogs of folic acid – Methotrexate
• Purine Salvage Pathway

• Conversion of purines from normal
turnover of cellular nucleic acids or
from diet
• Purine bases  nucleotides
• APRT – Adenine
phosphoribosyltransferase
• HGPRT – Hypoxanthine-guanine
phosphoribosyltransferase
• Purine Salvage Pathway

• Lesch-Nyhan Syndrome
• X-linked, recessive, inherited disorder
• Absence of HGPRT
• Inability of salvage guanine or
hypoxanthine
• Decreased IMP and GMP
• Increased De novo purine synthesis\
• Excess URIC ACID

• Neurologic symptoms
• Self mutilation
• Involuntary movements CHM060: BIOMOLECULES
• DEGRADATION OF PURINE
NUCLEOTIDES
• Degradation in the small intestine
• Pancreatic enzymes
• Mucosal enzymes
• Nucleosides and free bases
• Formation of Uric ACID
• Diseases of Purine Degradation

• GOUT
• Hyperuricemia
• Deposition of monosodium urate crystals
• ALLOPURINOL – inhibits xanthine oxidase
• Adenosine deaminase (ADA) deficiency

• Autosomal recessive
• A type of severe combined immunodeficiency (SCID)
• Accumulation of adenosine
• Adenosine  ribonucleotide/deoxyribonucleotide from
• Accumulation of dATP  inhibition of DNA synthesis
• Apoptosis of Lymphocytes
• PYRIMIDINE SYNTHESIS
• Ring is synthesized before being attached to
ribose-5-phosphate
• Synthesis of carbamoyl phosphate
• REGULATED STEP
• Synthesis of Orotic Acid

• Aspartate transcarbamoylase
• Dihydroorotase – closes the ring
• Dihydroorotate dehydrogenase – inner
mitochondrial membrane
• Other enzymes - cytosolic
• PYRIMIDINE SYNTHESIS
• OMP  UMP
• Synthesis of UTP and CTP
• Synthesis of TMP from dUMP
• Thymidylate synthase – uses N5,N10 –
methylene-FH4 as source of methyl
group
• PYRIMIDINE
DEGRADATION
• Pyrimidine ring is opened and
degraded to:
• Alanine
• Aminoisobutyrate
• NH4
• CO2
• Synthetic inhibitor of PYRIMIDINE synthesis

• Leflunomide
• Inhibit dihydroorotate dehydrogenase
• Methotrexate, Trimethoprim, pyrimethamine
• Inhibit dihydrofolate reductase (decrease in dTMP)
• 5-FU
• Inhibit thymidylate synthase
QUESTION
14. Which of the following can be absorbed by the
intestine in the absence of micelles?
A. Lipid-soluble vitamins
B. Lysophospholipids
C. Cholesterol
D. Short chain fatty acids
ADD A FOOTER 38
QUESTION
14. Which of the following can be absorbed by the
intestine in the absence of micelles?
A. Lipid-soluble vitamins
B. Lysophospholipids
C. Cholesterol
D. Short chain fatty acids
ADD A FOOTER 39
QUESTION
71. Which of the following are the end products of
digestion of triacylglycerol by pancreatic lipase prior to re-
esterification inside intestinal cells?
A. 3 free fatty acids and glycerol
B. 2-monoacylglycerol and 2 free fatty acids
C. 3-monoacylglycerol and 1 fatty acid
D. glycerol -3 phosphate and 3 fatty acids
ADD A FOOTER 40
QUESTION
71. Which of the following are the end products of
digestion of triacylglycerol by pancreatic lipase prior to re-
esterification inside intestinal cells?
A. 3 free fatty acids and glycerol
B. 2-monoacylglycerol and 2 free fatty acids
C. 3-monoacylglycerol and 1 fatty acid
D. glycerol -3 phosphate and 3 fatty acids
ADD A FOOTER 41
QUESTION
81. The end product of fatty acid synthesis de
novo prior to further elongation is:
A. stearic acid
B. lignoneric acid
C. palmitic acid
D. oleic acid
ADD A FOOTER 42
QUESTION
81. The end product of fatty acid synthesis de
novo prior to further elongation is:
A. stearic acid
B. lignoneric acid
C. palmitic acid
D. oleic acid
ADD A FOOTER 43
QUESTION
82. Which of the following is true of beta
oxidation of fatty acids?
A. occurs primarily in the cytosol and endoplasmic reticulum
B. carnitine transports fatty acyl-CoA from the cytosol into the
mitochondrial matrix where oxidation takes place
C. Acyl Carrier Protein (ACP) is required for the attachment of fatty acyl-
CoA
D. generates principally propionyl-CoA as final products for even number
fatty acids
ADD A FOOTER 44
QUESTION
82. Which of the following is true of beta
oxidation of fatty acids?
A. occurs primarily in the cytosol and endoplasmic reticulum
B. carnitine transports fatty acyl-CoA from the cytosol into the
mitochondrial matrix where oxidation takes place
C. Acyl Carrier Protein (ACP) is required for the attachment of fatty acyl-
CoA
D. generates principally propionyl-CoA as final products for even number
fatty acids
ADD A FOOTER 45
QUESTION
83. Ketogenesis in the liver occurs during this
metabolic condition:
A. increased beta oxidation of fats during prolonged

fasting and in diabetes mellitus
B. increased insulin and decreased glucagon levels
C. decreased activity of hormone sensitive lipase
D. excessive intake of carbohydrates and lipids in the diet
ADD A FOOTER 46
QUESTION
83. Ketogenesis in the liver occurs during this
metabolic condition:
A. increased beta oxidation of fats during prolonged

fasting and in diabetes mellitus
B. increased insulin and decreased glucagon levels
C. decreased activity of hormone sensitive lipase
D. excessive intake of carbohydrates and lipids in the diet
ADD A FOOTER 47
QUESTION
59. Prostaglandins are derived from:
A. Lignoceric Acid
B. Arachidonic Acid
C. Docosahexaenoic acid
D. Stearic Acid
ADD A FOOTER 48
QUESTION
59. Prostaglandins are derived from:
A. Lignoceric Acid
B. Arachidonic Acid
C. Docosahexaenoic acid
D. Stearic Acid
ADD A FOOTER 49
LIPIDS
• Most efficient way to carry energy

• High energy content
• Fatty Acid = building block
• the reason why most food products tastes
good
LIPID CLASSES
• FATTY ACID
• Building block • 2 properties
• TRIACYLGLYCEROLS • Insoluble in water
• Storage form
• WAXES • Soluble in nonpolar
• Protection solvents such as ether and
• PHOSPHOLIPIDS chloroform
• Membranes
• SPHINGOLIPIDS
• Membranes
• STEROIDS
• Membranes and hormones
FATTY ACIDS
• Alkyl chain with carboxylic acid

• Usually EVEN number of Carbons
• Can be either
• SATURATED
• UNSATURATED
• MONO/POLY
• CIS bond most common form
ω Fatty Acids are anti-inflammatory and have health
benefits
• Long chain ω3 FA
• α-linolenic acid (ALA) – plant oils
• Eicosapentaenoic acid (EPA) – fish oils
• Docosahexaenoic acid (DHA) – fish and algal oils
• Potential use for chronic inflammatory diseases
• Diets rich in ω3 are beneficial for:
• Cardiovascular diseases
• Cancer
• Rheumatoid arthritis
• Alzheimer’s disease
ARACHIDONIC ACID
STEROIDS
• Similar cyclic nucleus that

resemble phenanthrene
(A,B,C) to which a
cyclopentane ring (D) is
attached
• Steroids in the body
• Bile acids
• Adrenocortical hormones
• Sex hormones
• Vitamin D
• Cardiac glycosides
CHOLESTEROL
• Best known for its
association with heart
disease
• Widely distributed in all
cells particularly in
nervous tissue
• Major constituent of the
plasma membrane
• Essential Role:
• Precursor for steroids
ERGOSTEROL
• Occurs in plants and yeast

• Important source of
VITAMIN D
• Upon exposure to UV
light  ring B is opened
 forms Vit D2
FATTY ACID METABOLISM
• Degradation
• Triacylglycerols and
fatty acids
• Ketone Bodies
• Biosynthesis
• Fatty acids
ABSORPTION OF LIPIDS
• Lumen of small intestine:

• TAGs  FAs and monoacylglycerols
• Transport into enterocytes
• Converted back to TAGs
• Packaged with cholesterol:
chylomicrons
• Distribution to adipose tissues
LIPOLYSIS
• Adipose stores TAGs
• In fasting, exercise and stress
• FAs needed as fuel  lipolysis
• TAG  Lipolysis  for FAs to be used as fuel
• Activated by glucagon and epinephrine
• FAs are transported in the blood stream
• Albumin – carrier protein in the blood
• HEART and MUSCLE – primary users of FAs
FATTY ACID ACTIVATION
• FAs are activated before oxidation

• The ONLY STEP that REQUIRES ATP
• acyl-CoA synthetase (thiokinase)
• Occurs in the OUTER MITOCHONDRIAL
MEMBRANE
• Uses 2 equivalents of ATP
CARNITINE SHUTTLE
Carnitine
acyltrans
ferase I
• Acyl-CoA cannot readily cross the inner

membrane
• Transported using the CARNITINE SHUTTLE
• OUTER MITOCHONDRIAL MEMBRANE
• Conversion to ACYL CARNITINE by CAT I (Carnitine
Acyltransferase I)
Carnitine
Translocase
acyltransf
erase II
• transported by TRANSLOCASE to the
MITOCHONDRIAL MATRIX
• MATRIX
• ACYL CARNITINE conversion to Acyl-CoA by
CAT II
FATTY ACID OXIDATION
• FA
• broken down by oxidation to acetyl-CoA
• Breakdown of FA
• Each step involves Acyl-CoA derivatives
• Catalyzed by separate enzymes
• Requires NAD+ and FAD
• Generates ATP
• Aerobic process = REQUIRES OXYGEN
FATTY ACID OXIDATION
• Increase FA  starvation and Diabetes

Mellitus
• Generation of Ketone Bodies
• Acidic  in excess can lead to ketoacidosis 
FATAL
• Impaired FA Oxidation
• Hypoglycemia
ß-OXIDATION OF FATTY
• broken between the

α(2)- and β(3)-carbon
atoms
• 2 Carbons at a time are

cleaved
ß-OXIDATION OF FATTY ACID
• “Fatty acid oxidase”

• Collective term for enzymes that
catalyze the oxidation acyl-CoA to
acetyl-CoA
• Found in the mitochondrial matrix
or inner membrane adjacent to the
respiratory chain
• Generates large amounts of
reducing equivalents FADH2 and
NADH  ETC  ATP
• Four steps
1. Acyl-CoA dehydrogenase
(dehydrogenation)
• Reduction of FAD, C=C formation
2. Enoyl-CoA hydratase (hydration)
3. ß-hydroxyacyl-CoA
dehydrogenase (oxidation)
• Reduction of NAD+
4. Thiolase: production of acetyl-
CoA (thiolysis)
• Long chain fatty acid

• Even no. of carbons  degraded
completely to acetyl-CoA 
oxidized to CO2 and water via the
Krebs Cycle
• FOR SATURATED FA
• 1 cycle
• 1 NADH
• 1 FADH2
• 1 Acetyl-CoA
• Last cycle would produce additional 1 acetyl-CoA
• PALMITIC ACID (C16)

• (No. of carbons/2)-1 = (16/2) – 1 = 7 Cycles
• 7 NADH, and 7 FADH2 from the 7 cycles
• 8 molecules of Acetyl CoA by beta oxidation
• FOR UNSATURATED FA
• For 1 double bond = loss of 1 FADH2
• First step of ß-oxidation is skipped
• OLEIC ACID (18:1Δ9)

• (18/2)-1 = 8 cycles
• 8 NADH
• 8 FADH2 – 1FADH2 (one double bond) = 7 FADH2
• 9 Acetyl-CoA
• PRODUCES LARGE AMOUNTS OF ATP
• C16 – palmitate
• 7 cycles
• Per cycle
• 1 mol NADH = 2.5 mol ATP from ETC
• 1 mol of FADH2 = 1.5 mol ATP from ETC
4 mol of ATP per cycle
• From electron carriers = 7 cycles x 4 mol of ATP = 28 mol ATP

• 8 mol of Acetyl-CoA
• TCA
• 1 mol of acetyl-CoA  oxidized  10 mol of ATP
• 8 mol of acetyl-CoA x 10 mol of ATP/1 mol of
acetyl-CoA = 80 mol of ATP

• ELECTRON CARRIERS = 28 mol of ATP
• ACETYL-COA = 80 mol of ATP
108 mol ATP
• Acyl-CoA synthase = -2 mol ATP
106 mol ATP
FATES OF ACETYL-COA
KETOGENESIS
• Occurs under metabolic conditions with high rate of FA oxidation

• Lack of oxaloacetate in the cytosol for TCA to occur in the matrix
• LIVER MITOCHONDRIA – acetoacetate and ß-hydroxybutyrate
KETOGENESIS
KETONE BODIES SERVE AS A FUEL FOR
EXTRAHEPATIC TISSUES
• Heart and aerobic muscle love ketone

bodies
• Brain under starvation
• Conversion to acetyl CoA
• Acetoacetate
• Activated to acetoacetyl-CoA by 3-ketoacetyl-
CoA transferase
• Addition of CoA  cleaved by thiolase 
produces 2 mols of acetyl-CoA
KETONE BODIES SERVE AS A FUEL FOR
EXTRAHEPATIC TISSUES
KETONE BODIES IN DIABETES
• Diabetic Ketoacidosis
FATTY ACID SYNTHESIS
• Occurs in the CYTOSOL OF LIVER and ADIPOSE

• Animal tissues – limited capacity for desaturation of
FA
• Unsaturated FA
• Important for membrane fluidity
• High PUFAs in the diet – beneficial in preventing
coronary artery disease
• ESSENTIAL FATTY ACIDS needed to form

eicosaenoic (C20) FA for synthesis of other lipid
derived compounds in the body
• α-linolenic acid (ALA) – plant oils
• Eicosapentaenoic acid (EPA) – fish oils
• Docosahexaenoic acid (DHA) – fish and algal oils
• Immediate
substrate: AcCoA
• Mn2+, NADPH,
ATP, bioitin
• End Product: Free
palmitate
• Acetyl-CoA Sources
• GLUCOSE
• Glycolysis and PDH
• AMINO ACIDS – all 20 can be converted to fat
• Leu, Ile, Trp, Lys, Phe, Tyr  AcCoA
• Ala, Cys, Gly, Ser  pyruvate  AcCoA
• Asn, Asp, Met, Val, Arg, Glu, Gln, His, Pro 
CAC  oxaloacetate  pyruvate  AcCoA
• NADPH Source
• Pentose Phosphate Pathway
• Shunt of glycolysis
• Allows for the production of ribose for
nucleic acids
ACETYL CoA Activation
• MOST Acetyl CoA must be activated
• One will remain inactivated per FA
formed
• Conversion to malonyl CoA
• Catalyzed by Acetyl CoA carboxylase
• Multienzyme protein
• Contains:
• Biotin
• Biotin carboxylase
• Biotin carboxyl carrier protein (BCP)
• Carboxyl transferase
ACETYL CoA Activation
• Conversion to
malonyl CoA
• STEP 1:
carboxylation of biotin
involving ATP
• STEP 2: transfer of
carboxyl group to
AcCoa to form
malonyl CoA
FATTY ACID SYNTHESIS FROM MALONYL
CoA
• FATTY ACID SYNTHASE
ENZYME COMPLEX
• Multienzyme polypeptide
complex
• Homodimer of 2 polypeptide
chains
• Works in conjunction with
acyl carrier protein (ACP)
• Serve a similar function to CoA
• Contains pantothenic acid (Vit
B5)
QUESTION
For items 12-13: Mr. K is a male patient who complained of nape pains and headache, with a BP of
160/100
12. Lipid profile was determined which revealed elevated LDL cholesterol. This lipoprotein:
A. Is derived from the metabolism of HDL-cholesterol

B. Transports cholesterol from the peripheral tissues to the liver
(reverse cholesterol transport)
C. Is taken up by tissues through receptor mediated endocytosis
D. Functions as reservoir of apoprotein CII and apoprotein
ADD A FOOTER 96
QUESTION
160/100
12. Lipid profile was determined which revealed elevated LDL cholesterol. This lipoprotein:
A. Is derived from the metabolism of HDL-cholesterol

B. Transports cholesterol from the peripheral tissues to the liver
(reverse cholesterol transport)
C. Is taken up by tissues through receptor mediated
endocytosis
D. Functions as reservoir of apoprotein CII and apoprotein
ADD A FOOTER 97
QUESTION
160/100
13. The hypercholesterolemia which could be seen in this patient could be trated with an inhibitor of
the enzyme which catalyzes this rate limiting step of cholesterol biosynthesis:
A. Mevalonic acid kinase

B. Hydroxymethyl glutaryl CoA (HMGCoA reductase)
C. Cholesterol esterase
D. Squalene oxidase
ADD A FOOTER 98
QUESTION
160/100
13. The hypercholesterolemia which could be seen in this patient could be trated with an inhibitor of
the enzyme which catalyzes this rate limiting step of cholesterol biosynthesis:
A. Mevalonic acid kinase

B. Hydroxymethyl glutaryl CoA (HMGCoA
reductase)
C. Cholesterol esterase
D. Squalene oxidase
ADD A FOOTER 99
QUESTION
40. Bile acids are important in lipid digestion
because they:
A. emulsify lipids prior to action of enzymes

B. provide optimum pH of the enyzmes
C. promote reesterification of products of
tricacylglycerol digestion
D. facilitate packaging of lipids into chylomicrons
ADD A FOOTER 100
QUESTION
40. Bile acids are important in lipid digestion
because they:
A. emulsify lipids prior to action of enzymes

B. provide optimum pH of the enyzmes
C. promote reesterification of products of
tricacylglycerol digestion
D. facilitate packaging of lipids into chylomicrons
ADD A FOOTER 101
QUESTION
42. Which statement correctly describes the regulation
of the synthesis and uptake of cholesterol?
A. Cholesterol will increase the uptake of low density lipoproteins from the
circulation.
B. Upregulation of LDL receptors on the cell surface results in the activation of
HMG CoA reductase
C. Insulin activates HMG-CoA reductase by dephosphorylation of the enzyme.
D. Cholesterol, as a product of de novo synthesis, increases HMG-CoA
reductase synthesis and activity
ADD A FOOTER 102

QUESTION
42. Which statement correctly describes the regulation
of the synthesis and uptake of cholesterol?
A. Cholesterol will increase the uptake of low density lipoproteins from the
circulation.
B. Upregulation of LDL receptors on the cell surface results in the activation of
HMG CoA reductase
C. Insulin activates HMG-CoA reductase by dephosphorylation of the enzyme.
D. Cholesterol, as a product of de novo synthesis, increases HMG-CoA reductase
synthesis and activity
ADD A FOOTER 103

QUESTION
60. The biochemical defect in Type Ila Familial
Hypercholesterolemia:
A. Deficiency in the LDL receptors on the surface of

the cell membrane
B. Absent feedback inhibition of HMG Co reductase
C. Decreased synthesis of Lipoprotein Lipase
D. Increased conversion of VLDL to LDL
ADD A FOOTER 104
QUESTION
60. The biochemical defect in Type Ila Familial
Hypercholesterolemia:
A. Deficiency in the LDL receptors on the surface of

the cell membrane
B. Absent feedback inhibition of HMG Co reductase
C. Decreased synthesis of Lipoprotein Lipase
D. Increased conversion of VLDL to LDL
ADD A FOOTER 105
CHOLESTEROL
• Synthesized from cytosolic acetyl-
CoA
• Glucose – major source of acetyl-
CoA
• HMG-CoA reductase
• Rate limiting enzyme of cholesterol
biosynthesis
• inhibited by cholesterol, bile salts
• Induced by insulin
• Inhibited by statins
CHOLESTEROL
• CHOLESTEROL RING
• Cannot be degraed
• Forms bile salts for
exceretion
BILE SALTS
• PRIMARY BILE ACIDS
• Cholic acid
• Chenodeoxycholic acid
• Synthesized in the liver
• 7α-hydroxylase – regulatory enzyme
• Enter bile as glycine or taurine conjugates
• Further metabolized by intestinal bacteria
forming secondary bile acids
• SECONDARY BILE ACIDS
• Deoxycholic acid
• Lithocholic acid
BILE SALTS
• FATE OF BILE SALTS
• Primary
• Liver  secreted as bile  gallbladder
 intestine  aid in lipid digestion
• Secondary
• …intestine  primary bile deconjugated
 secondary bile salts
• RESORBED in the ileum and retured to
the liver via the ENTEROHEPATIC
CIRCULATION
• 95% recycled
• 5% feces
BLOOD LIPOPROTEINS
• Lipoproteins – serve to transport water insoluble TAGs and
cholesterol
• Composition
• Chylomicrons
• are the least dense of the blood lipoproteins because they have the most
triacylglycerol and the least protein.
• Deliver dietary lipids
• VLDL
• is more dense than chylomicrons but still has a high content of
triacylglycerol.
• Deliver endogenous lipids
BLOOD LIPOPROTEINS
• Lipoproteins – serve to transport water insoluble TAGs and
cholesterol
• Composition
• LDL
• has less triacylglycerol and more protein
• the highest content of cholesterol and its esters.
• Deliver cholesterol to cells
• HDL
• is the most dense lipoprotein.
• lowest triacylglycerol and the highest protein content
• Reverse cholesterol transport
DISORDERS OF PLASMA LIPOPROTEINS
•HYPOLIPOPROTEINEMIA
• Abetalipoproteinemia
• No chylomicrons, VLDL, or LDL are formed
because of defect in the loading of apo B with lipid.
• Rare
• blood acylglycerols low
• intestine and liver accumulate acylglycerols
• Intestinal malabsorption
• Early death avoidable by administration of large
doses of fat-soluble vitamins, particularly vitamin E.
• HYPOLIPOPROTEINEMIA
• Low or near absence of HDL
• Familial alpha-lipoprotein deficiency
• Tangier disease
• Fish-eye disease
• Apo-A-I deficiencies
• Tendency toward hypertriacylglycerolemia as a result of absence
of apo C-ll, causing inactive LPL
• Low LDL levels. Atherosclerosis in the elderly.
•HYPERLIPOPROTEINEMIA
• Familial lipoprotein lipase deficiency (type I)
• to deficiency of LPL, abnormal LPL, or apo C-ll
deficiency causing inactive LPL.
• Familial hypercholesterolemia (type IIa)
• Defective LDL receptors or mutation in ligand
region of apo B-100.
•HYPERLIPOPROTEINEMIA
• Familial type III hyperlipoproteinemia (broad
beta disease, remnant removal disease,
familial dysbetalipoproteinemia)
• Deficiency in remnant clearance by the liver
is due to abnormality in apo E.
• Familial hypertriacylglycerolemia (type IV)
• Overproduction of VLDL often associated
with glucose intolerance and
hyperinsulinemia.
THANK YOU!
Good luck
Study well!

BIOCHEMISTRY 2nd Session

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BIOCHEMISTRY 2nd Session

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BIOCHEMIST

6. Which of the following components are found in DNA

6. Which of the following components are found in DNA

• The smaller pyrimidine

• Derivatives of purines and

5. Which one is correct concerning purine and pyrimidine metabolism?

A. Purines degrade to CO2 and water

5. Which one is correct concerning purine and pyrimidine metabolism?

A. Purines degrade to CO2 and water

A. Inhibits PRPP synthase resulting to increased excretion of uric

A. Inhibits PRPP synthase resulting to increased excretion of uric

• SYNTHESIS OF PURINE NUCLEOTIDES

• SYNTHESIS OF PURINE NUCLEOTIDES

• Synthetic inhibitor of PURINE synthesis

• Purine Salvage Pathway

• Purine Salvage Pathway

• Excess URIC ACID

• Diseases of Purine Degradation

• Adenosine deaminase (ADA) deficiency

• Synthesis of Orotic Acid

• Synthetic inhibitor of PYRIMIDINE synthesis

A. increased beta oxidation of fats during prolonged

A. increased beta oxidation of fats during prolonged

• Most efficient way to carry energy

• Alkyl chain with carboxylic acid

• Similar cyclic nucleus that

• Occurs in plants and yeast

• Lumen of small intestine:

• FAs are activated before oxidation

• Acyl-CoA cannot readily cross the inner

• Increase FA  starvation and Diabetes

• broken between the

• 2 Carbons at a time are

• “Fatty acid oxidase”

• Long chain fatty acid

• PALMITIC ACID (C16)

• OLEIC ACID (18:1Δ9)

• PRODUCES LARGE AMOUNTS OF ATP

• PRODUCES LARGE AMOUNTS OF ATP

• Occurs under metabolic conditions with high rate of FA oxidation

• Heart and aerobic muscle love ketone

• Occurs in the CYTOSOL OF LIVER and ADIPOSE

• ESSENTIAL FATTY ACIDS needed to form

A. Is derived from the metabolism of HDL-cholesterol

A. Is derived from the metabolism of HDL-cholesterol

A. Mevalonic acid kinase

A. Mevalonic acid kinase

A. emulsify lipids prior to action of enzymes

A. emulsify lipids prior to action of enzymes

ADD A FOOTER 102

ADD A FOOTER 103

A. Deficiency in the LDL receptors on the surface of

A. Deficiency in the LDL receptors on the surface of

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