Thymine is a water-soluble micronutrient required to synthesize macronutrients like carbohydrates, proteins and fats.

1. Thymine
IRTIZA BINTI FAROOQ
FOOD SCIENCE AND
NUTRITION

2. content
 Metabolism
 Functions
 Sources
 Deficiency

3. How does vitamins function
 Vitamins form part of coenzymes that enables
enzymes to release energy from
carbohydrates, proteins and fats.

4. What is thiamine(B1)
 Thiamin is a vitamin, an essential micronutrient. It
is a water-soluble vitamin, which means it
dissolves in water and is carried to different parts
of the body but is not stored in the body.
 Thiamine is on the World Health Organization's
List of Essential Medicines.
 Within the body, the best-characterized form
is thiamine pyrophosphate(TPP), also called
thiamine diphosphate, a coenzyme in
the catabolism of sugars and amino acids

5. Thiamine
 Thiamine was first synthesized in 1926 as a coenzyme,
which was very helpful in researching its properties in
relation to beriberi, a vitamin b1 deficiency.
 as the first B vitamin discovered, so was termed vitamin
B1.
 Compared to other micronutrients, body stores of
thiamine are low. In addition, thiamine's half-life is only
10 to 14 days. Therefore, a continuous source of
dietary thiamine is necessary to prevent deficiency.

6. Metabolism
 It is an essential part of energy metabolism. This means that
thiamine helps convert carbohydrates into energy. Eating
carbohydrates increases the need for this vitamin, as your body
can only store about 30mg at a time due to the vitamins short
half-life.
 Thiamine metabolism begins in the extracellular space, being
transported by a thiamine transporter into the cell.
 Once in the intracellular space, thiamine is converted into
thiamine pyrophosphate through the enzyme thiamin
pyrophosphate kinase. Thiamine pyrophosphate is then
converted into thiamine triphosphate, again using the enzyme
thiamin pyrophosphate kinase .
 In the jejunum, thiamine is converted to thiamine
pyrophosphate(TPP), which is the main coenzyme form of
thiamine.

7. Metabolism
 Thiamine and TPP play important roles within
mitochondria in the decarboxylation of α-keto
acids to coenzyme A (CoA) moieties, an important
process in ATP synthesis. In short conversion of
pyruvate to acetyl coA.

8. Metabolism

9. hj
 The uptake of thiamine is enhanced
by thiamine deficiency, but can be reduced by
the presence of diabetes mellitus.
 Additionally, thiamine absorption is inhibited
by thiamine analogs (such as metronidazole),
ethanol, and diuretics (such as amiloride).
 Thiamine is mainly excreted in urine.

10. Functions
 Thiamin is important for the
growth, development, and
function of the cells in the body.
 TPP is a coenzyme in reactions
involved in myelin formation.
Muscles heavily depends on
thiamin.
 Thiamine may also have an
effect on nerve conduction and
transmission.
 Thiamine is involved in a wide
variety of the intricate
biochemical pathways
necessary for proper tissue and
organ function

11. Functions
 Thiamine plays a pivotal role in the pentose
phosphate pathway, which is not only an
alternate glucose metabolism pathway, but
also a major route for the synthesis of
several neurotransmitters, nuclic acids, lipids,
amino acids, steroids, and glutathione.

12. Dietary sources
 It is found in food and
commercially synthesized to
be a dietary
supplement or medication.
 Food sources of thiamine
include whole
grains, legumes, and some
meats and fish. Grain
processing removes much of
the thiamine content, so in
many
countries cereals and flours a
re enriched with thiamine.

13. Deficiency
 People who are malnourished, who eat polished, refined cereals
and those who derive most of their energy from empty k calorie
items, like alcohol, risk thiamine deficiency.
 Prolonged thiamine deficiency can result in the disease beriberi.
Symptoms of beriberi includes damage to nervous system, the
heart and the other muscles.
 It also can cause paralysis as it participates in nerve processes.
 In alcoholics the most serious deficiency causes wernicke-
korsakoff. Symptoms include disorientation, loss of short term
memory, jerky eye movement, and staggering gait.
 Thiamine deficiency can lead to autonomic nervous system
dysfunction, abnormal vagal tone, and lower acetylcholine
synthesis.

15. References
 Lehninger, A.L. Lehninger principles of biochemistry (4th ed.) (2005).
New York: W.H Freeman.
 Manzetti S, Zhang J, van der Spoel D: Thiamin function, metabolism,
uptake, and transport. Biochemistry. 2014 Feb 11;53(5):821-35. doi:
10.1021/bi401618y. Epub 2014 Jan 31.
 Pubmed: 24460461
 Nosaka K, Onozuka M, Kakazu N, Hibi S, Nishimura H, Nishino H, Abe T:
Isolation and characterization of a human thiamine pyrophosphokinase
cDNA. Biochim Biophys Acta. 2001 Jan 26;1517(2):293-7. doi:
10.1016/s0167-4781(00)00247-5.
 Pubmed: 11342111
 Zhao R, Gao F, Goldman ID: Molecular cloning of human thiamin
pyrophosphokinase. Biochim Biophys Acta. 2001 Jan 26;1517(2):320-2.
doi: 10.1016/s0167-4781(00)00264-5.
 Pubmed: 11342117