basic information

1. NIACIN

2. DISCOVERY
• Pellagra was first observed in 1900’s in U.S –
families whose diet is largely based on corn.
• Children – no pellagra seen- high intakes of
meat and milk.
• Pellagra related to food factor.
• Goldberg experiment – 12 convicts – corn meal,
corn starch, rice, sweet potato and pork fat.
• Administration of dried meat or liver cured
pellagra.
Thus niacin was discovered by
Goldberger in 1928.
• Other names are nicotinic acid, P.P, anti
pellagra vitamin, and vitamin-B 3.

3. CHEMISTRY
Exists in 2 forms
Nicotinic acid Nicotinamide
mol wt is 123 mol wt. is 122
• Niacin is a pyridine derivative.
• Structurally it is pyridine 3 – carboxylic acid.
• Water soluble, stable to acid and heat.
• White powder when crystallized.
• Coenzymes NAD and NADP – oxidation – reduction rxn’s
- enzymes oxidoreductases
Nicotinic acid

4. Precursor role of tryptophan
Q 1. Why did milk, which is low in niacin cure or prevent
pellagra?
Q 2. Why was pellagra so common in families subsisting on
diets high in corn?
Key discovery – tryptophan can be used by
the body to make niacin.
Corn based diet- low
in both tryp and niacinMilk – high in tryptophan

6. • Nicotinamide –
niacin
• PRPP ( phospho
ribosyl pyro
phosphate) –
ribose phosphate
• ATP – AMP
moiety
• Glutamine –
amide group

7. NAD and NADH
electron acceptor hydrogen donor
Catabolism rxn’s
𝐴𝐻2 + 𝑁𝐴𝐷+ A + NADH + 𝐻+
Example
ETC
ATP

8. NADP and NADPH
• Anabolism or bio synthesis rxn’s
Examples – biosynthesis of fatty acids
and steroids.
Eg. 1
Eg. 2
NADP - hydrogen donor

9. Digestion absorption and storage
• NAD / NADP are digested by nucleotide pyrophosphatases
present in pancreatic and intestinal secretion.
• Nicotinamide and niconitate are absorbed from stomach and
small intestine - transported in blood - uptake by cells.
Excretion : Excreted as N methyl nicotinamide, nicotinic acid N-
oxide, N1 – methyl- 2- pyridone -5 – carboxamide etc
Storage sites : Liver, Kidney, Heart, and skeletal muscles – high
concentrations of NAD

10. RDI
Very often niacin equivalents are used while expressing RDA
1 NE = 60 mg of tryptophan
Adequate intake = 15 – 20 mg
GROUP CATEGORY/ AGE N . E (mg/d)
MEN 16-21
WOMEN 12-16
Pregnant +2
Lactating 0-6 m
6-12m
+4
+3
INFANTS 0-6m 710µg/kg
6-12 650µg/kg
CHILDREN 1-9 yr 8-13
BOYS 10-17yr 15-17
GIRLS 10-17yr 13-14

11. Food Sources
• Meat, liver, fish, yeast and
diary products – major
sources of niacin and
tryptophan.
Other are peanuts, dried beans,
and peas, whole grains, treated
millets like corn, roasted coffee
beans( trigonelline), enriched
breads an cereals.

12. DEFICIENCY
• Deficiency of niacin causes Pellagra( Italian : rough skin).
• This disease involves skin, gastrointestinal tract, and
central nervous system.
Symptoms : 4 D’s
Dermatitis, Diarrhea, Dementia if not treated Death.
Risk of deficiency :
Mostly seen among people whose staple diet is corn and
maize.

13. OTHER EFFECTS
Pharmacological use : Niacin and its related derivatives
when given in daily doses of 1 to several gm treats
hyperlipidemia
Possible effects stated are:
• Lowers LDL cholesterol and Lp(a) conc.
• Increases HDL cholesterol.
HYPERVITAMINOSIS
• At intake levels of 1000 to
2000mg leads to skin flushing and
itching as nicotinic acid acts as
vasodilator.
• Other effects are G.I upset,
hyperglycemia, liver damage, etc.
• So medical supervision is very
important.