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Vitamins B1, B2, B3, biotin –
energy-releasing vitamins
Active form of Thymine (Thymine
pyrophosphate- TPP)
N
N
H3C
NH2
CH2
S
N
CH3
CH2 CH2O PP
reactive carbon atom
pyrimidine thiazole ring
pyrophosphate
TPP is required for energy releasing
reactions such as:
 Oxidative decarboxylation of α-ketoacids:
 E.g. Co-enzyme for pyruvate
dehydrogenase (PDH)
COO
C O
CH3
CoA-SH
SCoA
C O
CH3
+ CO2
NAD+
NADH
TPP
PDH
Pyruvate Acetyl CoA
E.T.C.
(3 ATP)
Metabolism of branching amino acids -
Valine:
CH3 CH
CH3
H
C
NH2
COO CH3 CH
CH3
C
O
COO
ketoisovaleric acid
CO2
KDH
(TPP)
NADH
NAD+
CH3 CH
CH3
C
O
SCoA
isobutyryl CoA
succinyl CoA
TCA
Role in the transmission of nerve
impulse
 TPP acts as a
phosphate donor for
phosphorylation of
the nerve membrane
sodium transport
channel.
THIAMINE DEFICIENCY
 Most dietary deficiency of
thiamine is the result of:
 (i) poor dietary intake
 (ii) diet high in
carbohydrates only
 (iii) alcoholism
 (iv) cancer, chronic illness
 tea, coffee, certain
seafoods may contain
thiaminases that
destroyed the vitamin and
lead to deficiency.
Beriberi
 “Beriberi” a neurological disorders, that
was endemic in the polish-rice eating
countries.
Types of “beriberi”
Dry Wet
Infantile
Adult Adult In first year
of life
Polyneuritis
(damage of peripheral
nerves)
Cardiac failure
& edema
In late stage,
muscular atrophy results.
May become paralysis
Cardiovascullar
problems
Wernike-Karsakoff syndrome:
 Seen primary in association with
chronic alcoholism and is due to
dietary insufficiency or impaired
intestinal absorption of vitamin
B1.
 Characterized by apathy, loss of
memory and rhythmical and fro
movements of eye balls.
It forms two biological coenzymes:
 Flavin Mononucleotide (FMN)
 Flavin Adenine Dinucleotide (FAD).
– FMN and FAD help in the oxidation-reduction
reactions.
– FMN and FAD are the coenzymes of enzymes
which are involved in the synthesis of ATP in
mitochondria (TCA cycle, ETC).
DEFICIENCY OF VITAMIN B2
 Inflammation of lips,
stomatitis.
 Inflammation and
vascularization of
cornea, photophobia
(intolerance of light),
cataract formation.
Structure
N
C
O
OH
N
C
O
NH2
nicotinic acid
nicotinamide
(coenzyme of NAD+
,
NADP+
)
R
Deficiency of Niacin causes Pellagra.
 Pellagra is a disease involving the skin,
gastrointestinal tract and central nervous
system.
 Symptoms of pellagra 3 Ds:
 Dermatitis (lesion of skin of face, neck, thick and
scaly skin).
 Dementia (headache, depression, forgetfulness,
insomnia (loss of sleep), anxiety.
 Diarrhea
 Death (4th D) is not treated.
CLINICAL USES OF NIACIN
 It is used in the
treatment of
hyperlipidemia
 Niacin strongly
inhibits lipolysis in
adipose tissues
 decrease lipogenesis
in the liver
Biotin
 SOURCES:
 Present in almost all
foods particularly in
liver, milk, egg yolk,
chocolate
 Intestinal bacteria
also supply biotin in
large proportion.
Structure
Biological role
– Biotin is a coenzyme of carboxylase.
– It helps in the incorporation of carbon dioxide
(CO2) – CO2-“fixation” reaction.
COO
C O
CH3
CO2 COO
C O
CH2
COO
biotin
pyruvate
oxaloacetate
(TCA cycle
energy providing)
Biotin involves in the following
reactions:
 Purine synthesis
 Fatty acids synthesis
 Propionate convertion to succinate (TCA
cycle)
DEFICIENCY:
– The deficiency of biotin
may result from:
 The destruction of intestinal
bacteria by sulfonamide
drugs.
 The inadequate intake of egg
white which contains the
protein avidin (interfere
absorption of biotin) in
association with diarrhea in
case of infants.

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Vitamins of B group.ppt and it's function metabolism

  • 1. Vitamins B1, B2, B3, biotin – energy-releasing vitamins
  • 2.
  • 3. Active form of Thymine (Thymine pyrophosphate- TPP) N N H3C NH2 CH2 S N CH3 CH2 CH2O PP reactive carbon atom pyrimidine thiazole ring pyrophosphate
  • 4.
  • 5. TPP is required for energy releasing reactions such as:  Oxidative decarboxylation of α-ketoacids:  E.g. Co-enzyme for pyruvate dehydrogenase (PDH) COO C O CH3 CoA-SH SCoA C O CH3 + CO2 NAD+ NADH TPP PDH Pyruvate Acetyl CoA E.T.C. (3 ATP)
  • 6. Metabolism of branching amino acids - Valine: CH3 CH CH3 H C NH2 COO CH3 CH CH3 C O COO ketoisovaleric acid CO2 KDH (TPP) NADH NAD+ CH3 CH CH3 C O SCoA isobutyryl CoA succinyl CoA TCA
  • 7. Role in the transmission of nerve impulse  TPP acts as a phosphate donor for phosphorylation of the nerve membrane sodium transport channel.
  • 8. THIAMINE DEFICIENCY  Most dietary deficiency of thiamine is the result of:  (i) poor dietary intake  (ii) diet high in carbohydrates only  (iii) alcoholism  (iv) cancer, chronic illness  tea, coffee, certain seafoods may contain thiaminases that destroyed the vitamin and lead to deficiency.
  • 9. Beriberi  “Beriberi” a neurological disorders, that was endemic in the polish-rice eating countries.
  • 10. Types of “beriberi” Dry Wet Infantile Adult Adult In first year of life Polyneuritis (damage of peripheral nerves) Cardiac failure & edema In late stage, muscular atrophy results. May become paralysis Cardiovascullar problems
  • 11. Wernike-Karsakoff syndrome:  Seen primary in association with chronic alcoholism and is due to dietary insufficiency or impaired intestinal absorption of vitamin B1.  Characterized by apathy, loss of memory and rhythmical and fro movements of eye balls.
  • 12.
  • 13.
  • 14. It forms two biological coenzymes:  Flavin Mononucleotide (FMN)  Flavin Adenine Dinucleotide (FAD). – FMN and FAD help in the oxidation-reduction reactions. – FMN and FAD are the coenzymes of enzymes which are involved in the synthesis of ATP in mitochondria (TCA cycle, ETC).
  • 15. DEFICIENCY OF VITAMIN B2  Inflammation of lips, stomatitis.  Inflammation and vascularization of cornea, photophobia (intolerance of light), cataract formation.
  • 16.
  • 18.
  • 19. Deficiency of Niacin causes Pellagra.  Pellagra is a disease involving the skin, gastrointestinal tract and central nervous system.  Symptoms of pellagra 3 Ds:  Dermatitis (lesion of skin of face, neck, thick and scaly skin).  Dementia (headache, depression, forgetfulness, insomnia (loss of sleep), anxiety.  Diarrhea  Death (4th D) is not treated.
  • 20. CLINICAL USES OF NIACIN  It is used in the treatment of hyperlipidemia  Niacin strongly inhibits lipolysis in adipose tissues  decrease lipogenesis in the liver
  • 21. Biotin  SOURCES:  Present in almost all foods particularly in liver, milk, egg yolk, chocolate  Intestinal bacteria also supply biotin in large proportion.
  • 23. Biological role – Biotin is a coenzyme of carboxylase. – It helps in the incorporation of carbon dioxide (CO2) – CO2-“fixation” reaction. COO C O CH3 CO2 COO C O CH2 COO biotin pyruvate oxaloacetate (TCA cycle energy providing)
  • 24. Biotin involves in the following reactions:  Purine synthesis  Fatty acids synthesis  Propionate convertion to succinate (TCA cycle)
  • 25. DEFICIENCY: – The deficiency of biotin may result from:  The destruction of intestinal bacteria by sulfonamide drugs.  The inadequate intake of egg white which contains the protein avidin (interfere absorption of biotin) in association with diarrhea in case of infants.