Vitamin B3, also known as niacin, is an essential vitamin that plays a key role in many metabolic processes in the body. It is found in a variety of foods like meat, fish, eggs, nuts, and whole grains. A deficiency in niacin can cause pellagra, with symptoms of dermatitis, diarrhea, dementia, and even death. Treatment involves increasing dietary intake of niacin through foods or supplements. Maintaining a balanced diet with adequate protein and B vitamins can help prevent niacin deficiency diseases.

1. VITAMIN B3
PRESENTED BY :
SMRUTI KUDALKAR
GUIDED BY :
Ms. JEGGHNA CHHEDA.

2. VITAMIN B3- NIACIN
Introduction
 Niacin is the generic term for nicotinamide
and nicotinic acid
 Obtained by the oxidation of nicotine
 is an organic compound with the
formula C6H5NO2
 Simple derivative of pyridine
 White crystalline substance
 Water soluble
 Resistant to heat, oxidation & alkalis
 One of the most stable vitamin
 Can be easily synthesised commercially

3. Structure:
Niacin has a carboxyl group (COOH) at the 3-position,
whereas, in nicotinamide the carboxyl group is
replaced by a carboxamide group (CONH2)

4. Biosynthesis:
 The liver can synthesize niacin from the essential amino acid
tryptophan, requiring 60 mg of tryptophan to make one mg of
niacin.
Tryptophan (in presence of Fe)
Kynurenine ( NADPH NADP)
Quinolinic acid
Nicotinic acid Mononucleotide(NMN)
NAD
Niacin(Nicotinamide)

5. Metabolism:
 The de novo synthesis of NAD and
NADPH occurs from quinolinic acid, a
metabolite of tryptophan.
 The conversion of tryptophan to niacin
depends on amount of tryptophan and
niacin ingested and the Pyridoxine
status. (60 mg of tryptophan = 1 mg of
niacin)
 Dietary protein deficiency changes the
profile of urinary metabolites as there are
changes in the amount of tryptophan
being converted into niacin.

6. Absorption, Transport &
Storage:
• Nam and NA are absorbed in the stomach
and SI by carrier mediated facilitated
diffusion.
• Both are transported in the plasma in free
solution and each is taken up by most
tissues through passive diffusion, although
some tissues like erythrocytes, kidney and
brain, have a transport system also for NA.
• Niacin is retained in the tissues by being
converted into NAD and NADPH.

7. Functions:
 Niacin is required by all cells. It plays a vital role
in the release of energy from all energy yeilding
nutrients-CHO, fat, protein,alcohol.
 Also required for the synthesis of protien, fat &
5C sugars needed for the formation of DNA &
RNA.
 The biochemical role of niacin is to form part of
coenzymes NAD & NADP require by many of the
key pathways of the metabolism.
 Coenzymes NAD and NADPH are electron
carriers of cells. NAD is primarily involve in
catabolic reactions whereas, NADP functions
mainly in anabolic reactions. They are
coenzymes for more than 200 enzymes
reactions.

8.  Some of the reactions where niacin in the form of
NAD is involved are :
1. Conversion of lactate to pyruvate in glycolytic pathway.
2. Glyceradehyde-3-PO4 to 1, 3 biphosphoglycerate in
glycolytic pathway.
3. In biological oxidation reduction complex.
4. α- ketoglutarate to succinyl CoA in TCA cycle.
5. Malate to oxaloactetate in TCA cycle.
 Niacin in the form of NADP is involved in the
following:
1. Glucose-6-PO4 to 6-Phospho gluconolactone in HMP
stunt.
2. 6-phospho gluconate to 3 keto-6 phosphogluconate in
HMP stunt.
 Thus they play an important role in mechanisms for
DNA repair and gene stability and therefore
influence cancer risk.

9. Sources
Niacin is found in variety of foods-
Animal products like milk, eggs,
poultry, fish, beef
Fruits & vegetables: avocado, potato,
leafy vegetables
Seeds : groundnut, almonds, whole cereals, pulses

10. Recommended dietary
allowances
 Niacin requirement is related to energy intake. For
every 1000 kcal intake, 6.6 mg of niacin is to be taken.
 Infants
 0 - 6 months: 2 mg/day
 7 - 12 months: 4 mg/day
 Children
 1 - 3 years: 6 mg/day
 4 - 8 years: 8 mg/day
 9 - 13 years: 12 mg/day
 Adolescents and Adults
 Males age 14 and older: 16 mg/day
 Females age 14 and older: 14 mg/day
 Specific recommendations depend on age, gender, and
other factors (such as pregnancy). Women who are
pregnant or breast-feeding need higher amounts

11. Deficiency
 Slight deficiency of niacin can lead to irritability, poor
concentration, anxiety, fatigue, restlessness and
depression.
 Severe deficiency:
 PELLAGRA: caused by decreased intake of niacin
or tryptophan and possibly by excessive intake
of leucine.
 It occurs in the middle age population 20-50 where
both the sexes are equally affected.
 Pellagra is classically described by "the four Ds"
 Dermatitis- cracked skin, pigmented, scaly
dermatitis
 Dementia- involves CNS leads to confusion,
disorientation and neuritis
 Diarrhea and other digestive disturbances

12. Symptoms
 Clinical features: loss of weight & incresing debility.
 Diarrhoea & mental changes are not present in
mild deficiency.
 Dermal lesions: photo sensitive rash seen on
exposed body surface like lower & upper
extremities, face & neck.
 On the neck, the lesions appear in the form of a
necklace called Casal’s necklace.

13. Symptoms contd.
 Gastrointestinal changes: the mucous
membrane is inflammed resulting in severe
glossitis , stomatitis, oesophagitis, gastritis
& entertis. The inflammation can produce
bloody diarrhoea.
 Neurological manifestation: higher mental
functions are deranged in pellagra.
Insomnia occurs. As the disease
progresses it can manifest in disorientation,
hallucination & delirium.
 Acute encephalopathy characterised by
clouding of conciousness occurs.

14. Treatment
 Pellagra can be cured by a good diet
containing adequate amounts of protien,
tryptophan and/or niacin as well as other
members of B-complex group of vitamins.
 A moderately severe case requires nicotinic
acid or amide in doses of 100-300 mg/day
orally.
 Mental symptoms respond within 24-48 hours
& the dermal lesions require 3-4 weeks of
therapy.
 Most cases of pellegra require riboflavin &
pyridoxine particularly for neurological
manifestation.
 Oral terapy is satisfactory in all cases except
in those with very severe diarrhoea.

15. Prevention
 Pellagra can be prevented by the
following measures:
1. Replacing sorghum with other cereals.
2. Consuming sorhgum with good quality
protiens.
3. Fortifying bread with niacin.
4. Distributio of yeast & niacin tablets as
public health programme.
5. Developing low leucine strains of
sorghum.
6. Including groundnuts in every day diet.