ERRATA FOR BIOCHEMISTRY NEET PG NOTES 2020

Typographical/Formatting Errors

Unit IV Amino Acid and protein

Page 116
In Transaminases,
In Point no 2.:
δ-amino group should be changed as e-amino group

Unit V -Lipids

Page 160
In box: KETONE BODY UTILIZATION,
Under THIOPHORASE,
In second bullet, Line should be read as:
“CoA is added without using energy”

Page 167
In box: Cholesterol synthesis
RLE is “HMG-CoA reductase” instead of “HMG CoA synthase”
Refer to Corrected diagram of pathway on next page
CHOLESTEROL SYNTHESIS

2 Acetyl CoA (2C)

Thiolase

Acetoacetyl CoA (4C)

HMG-CoA synthase

HMG CoA (6C)

HMG-CoA Reductase (RLE) Θ Statins, Bile acids, Cholesterol

Mevalonate (6C) Farnesyl PPi Uses:

1. Synthesize coenzyme Q

Farnesyl PPi (15C) 2. Synthesize Dolichol PPi which is

required for N- glycosylation of
proteins
Squalene (30C)

Lanosterol (30 C) 1st cyclic compound formed

Cholesterol (27 C)
 Missing Notes
(Video-Lipoproteins, time 16:27- 22:43)

Lipoprotein lipase vs Hormone sensitive lipase

Lipoprotein Lipase
• Present in endothelium cells
• Anabolic enzyme
• Activated by insulin only in
capillary bed of adipose
tissue
• Breaks TG present in
chylomicrons and VLDL
when they pass through
adipose tissues.
Hormone sensitive lipase
• Present inside the adipose tissue cells
• Catabolic enzyme
• Inhibited by insulin but activated by
glucagon, epinephrine and thyroid
hormones
• Break TG in to fatty acid and
glycerol but cannot break FA at
second position of TGs.

Hormone sensitive lipase

Activators Inhibitors
• Glucagon • Insulin
• Thyroxin • Nicotinic acid (high doses of niacin
• Catecholamine are used as anti-hyperlipidemic
• ACTH drug)
• TSH • Prostaglandin E (PGE)
 Missing Notes
(Video-Lipoproteins, Time 45:50- 51:45)

LCAT ACAT
• Lecithin Cholesterol Acyl • Acyl-CoA Cholesterol Acyl
Transferase Transferase
• Present in HDL in blood • Present inside the adipose
vessels tissue cells

LCAT deficiency

Partial deficiency Complete deficiency

• Norum’s Disease • Fish eye Disease
• Severe hemolytic anemia and • c/f are same as Norum’s
End State Renal Disease disease but No hemolytic
(ESRD) anemia or ESRD

Norum Disease

LCAT
Cholesterol + lecithin Ch ester + lysolecithin
absent
(both Increased) (both Decreased)

C/f
• Causes ESRD
• Excess free cholesterol ® deposited in cornea ® Opacification
• Hemolytic anemia
Electrophoresis of Lipoproteins

Missing Notes
(Video-Lipoproteins, time 1:02:05- 1:04:34)

HYPOLIPOPROTEINEMIA
Abetalipoproteinemia
• Absent beta lipoproteins
• defect in absorption of lipids due to defective transport protein in
intestine ® absent or decreased beta-lipoproteins (LDL, VLDL, IDL,
chylomicrons) due to
• leads to defective absorption of fat-soluble vitamins
• Vitamin K deficiency leads to bleeding manifestations
c/f
1. Acanthocytosis (crenated RBCs)
2. Neurological problems
3. Steatorrhea
 Missing Notes
(Video-fatty acid synthesis, time 14:30- 21:13)

Elongation of fatty acid

® Upto 10 carbon fatty acid is made in cytoplasm by normal denovo FA
synthesis process.
® Further elongation of FA chain (upto C-24) is done by fatty acyl
elongase enzymes.
® Occurs in ER.
® Both NADH or NADPH can be used (NADPH is preferred).
® Includes loading, condensation and reduction steps.
® C-22 and C-24 FAs are specially required in brain for the formation
of sphingomyelin.

Desaturation of fatty acid

® Occur in liver ER
® Done by desaturase
® Enzymes doing desaturation are D4, D5, D6 and D9 destaurases
® Create double bond at D4, D5, D6 and D9 positions
® Humans do not have enzymes to create double bond beyond D9
position.
® So, the fatty acid containing double bond beyond D9 positions (PUFAs)
are need to be obtained in diet as essential fatty acids.

Formation of Triglycerides (TG)

TG = 3FAs + 1 Glycerol-3-P

Sources of Glycerol-3-P
 Gly-3-P dehydrogenase
1. DHAP Glycerol-3-P
(In liver and adipose tissues)

Glycerol kinase
2. Glycerol Glycerol 3-P
(only in liver)

As, DHAP can be obtained from glucose during glycolysis

So, Adipose tissue strictly depend on glucose uptake for TG synthesis

Missing Notes
(Video-genetic disorders, time 9:40- 15:35)

Inversion and Translocation

Inversion- alteration in the position of genes within the same chromosomes

Two Types:

Paracentric and Pericentric

Para- exchange on the same side of centromere.
Peri- exchange on the different side of centromere

Isochromosome: Special type of inversion

® Axis of division is perpendicular to normal axis
® Both short arms will be joined and lost
® Both long arms joined together and retained
 Centromere
Will be
Perpendicular lost
axis of division usually

Isochromosome
Normal axis (both arm same)
of division

Paracentric Pericentric
inversion inversion
Isochrosomes

Translocation: Exchange of gene material between two different

chromosomes e.g. T (8, 14) Burkitt lymphoma.
Balanced- If same amount of genetic material is exchanged
Unbalanced- If different amount of genetic material is exchanged

Special translocation: Robertsonian translocation

® Both short arms join together and both long arms join together.
® One goes to one cell and another goes to aa different cell.

Burkitt’s Lymphoma Robertsonian Translocation

Ch8 Ch8

Ch B Ch A
Ch14 Ch14
Ch A Ch B

Goes to
another
cell

Normal non- Goes to

Normal Burkitt’s one cell
homologus
Chromosomes Lymphoma
Chromosomes
 Missing Notes
(Video-genetic disorders, time 27:23- 31:09)

Trinucleotide repeat expansion

® Change in number of trinucleotide (e.g ACG) sequence repeats.

(A C G A C G -----------)n (A C G A C G ----------- )n
Mutation
n = 100 n = 200

® Causes severe neurological defects

e.g.
Huntington disease,
Fragile X syndrome
Friedrich ataxia,
Myotonic dystrophy

Germline mosaicism
® Parents not affected i.e. no defective alleles in parents
® Mutation occur after zygote is formed (postzygotic mutation in child)
® can be transmitted to next progeny
® Child affected first will have normal somatic cells but germ cell will
have the mutated gene.