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Water Soluble Vitamins
By
Dr.M.Anuswaru
THIAMINE (Vitamin B1)
• Also called as Antiberiberi factor, antineuritic
vitamin.
• It is involved in carbohydrate, fat , aminoacid
and alcohol metabolism.
• Free thiamine is a basic substance and
contains
(a) a pyrimidine, and
(b)a thiazole ring.
• It contains sulphur(sulphur containing
vitamin).
• The active coenzyme form of thiamin, vitamin
B1, is thiamin pyrophosphate (TPP) . It is
formed by addition of two phosphate groups,
by thiamine pyrophosphate transferase.
THIAMINE (Vitamin B1)
Sources
• Aleurone layer of cereals (food grains) is a rich
source of thiamine. Therefore, whole wheat
flour and unpolished hand pound rice have
better nutritive value than completely polished
refined foods.
• Liver, meat and eggs supply considerable
amounts. Ham/pork meats are particularly rich.
Biosynthesis :
• Synthesized by plants, yeasts and bacteria.
• Not synthesized by human beings, hence
should be supplied in diet.
• Intestinal bacterial flora can synthesize the
vitamin.
• There can be a substantial loss of thiamine in
cooking above 100degrees.
Absorption
• Free thiamine is absorbed readily from the
small intestine.
• Bulk of the dietary vegetable thiamine is in the
“free” form. In tissues, it is actively
phosphorylated to form Thiamine
pyrophosphate (TPP) in Liver, and to a lesser
extent in other tissues like muscle, brain and
RBC Cells.
Storage
• Capacity to store is limited.
• It is present in both free and combined forms
in heart (highest concentration), Liver and
kidneys.
• In lower concentration in skeletal muscle and
brain.
• Total amount of Thiamine in body is approx.
25 mg.
Recommended Daily Allowance of
Thiamine
• It depends on calorie intake (0.5 mg/1,000
calories).
• Requirement is 1.5–2 mg/day.
• Actual requirement is related more directly to
carbohydrates content of diet than to calorie
value of diet.
Requirements Increases in
• Anoxia-shock and hemorrhage, Serious illness
and injury, During prolonged administration of
broad-spectrum oral antibiotics, Increased
calorie expenditure like fever,
hyperthyroidism, Increased carbohydrate
intake, Increased alcohol intake, and
pregnancy and in lactation.
Metabolic Role of Thiamine
• Pyruvate dehydrogenase: The coenzyme form
is thiamine pyrophosphate (TPP). It is used in
oxidative decarboxylation of alpha-keto acids,
e.g. pyruvate dehydrogenase catalyzes the
breakdown of pyruvate, to acetyl-CoA, and
carbon dioxide.
• Alpha-ketoglutarate dehydrogenase: requires
TPP is the oxidative decarboxylation of alpha-
ketoglutarate to succinyl- CoA and CO2.
α-ketoglutarate succinyl- CoA + CO2
• Transketolase: in the hexose monophosphate
shunt pathway of glucose.
• B1 is also required in amino acid Tryptophan
metabolism for the activity of the enzyme
Tryptophan pyrrolase.
• Also acts as a coenzyme for mitochondrial
branched-chain α-ketoacid decarboxylase which
catalyzes oxidative decarboxylations of branched-
chain α-ketoacids formed in the catabolism of
valine, Leucine and Iso-leucine.
• The main role of thiamine (TPP) is in carbohydrate
metabolism. So, the requirement of thiamine is
increased along with higher intake of carbohydrates
Deficiency Manifestations of Thiamine
• The deficiency of thiamine produces a
condition called beriberi. It is characterized by
the following manifestations
• CV manifestations: These include palpitation,
dyspnea, cardiac hypertrophy and dilatation,
which may progress to congestive cardiac
failure.
• Neurological manifestations: These are
predominantly those of ascending,
symmetrical, peripheral polyneuritis.
• These neurological features may be
accompanied occasionally by an acute
polyencephalitis which is then called as
Wernicke’s encephalopathy. Carl Wernicke in
1894 and Sergiei Sergievich Korsakoff in 1887
described the condition.
• Clinical features are those of encephalopathy
(ophthalmoplegia, nystagmus, cerebellar
ataxia) plus psychosis. It is seen only when the
nutritional status is severely affected.
• GI symptoms: Amongst these, anorexia is an
early symptom. There may be gastric atony,
with diminished gastric motility and nausea;
fever and vomiting occur in advanced stages.
Types of beri beri
• Dry beriberi: Central nervous system (CNS)
manifestations are the major features.
Peripheral neuritis with sensory disturbance
leads to complete paralysis. It is not
associated with edema.
• Wet beriberi: Here cardiovascular
manifestations are prominent. Edema of legs,
face, trunk and serous cavities are the main
features.
• Infantile beriberi: It occurs in infants born to
mothers suffering from thiamine deficiency.
Restlessness and sleeplessness are observed.
Absence of deep tendon reflexes.
• Thiamine deficiency is manifested as
horizontal ridges in nails.
• Polyneuritis: It is common in chronic
alcoholics.
• Alcohol inhibits intestinal absorption of
thiamine, leading to thiamine deficiency.
• Thiamine deficiency in alcoholism may cause
impairment of conversion of pyruvate to
acetyl CoA. The result is increased plasma
concentration of pyruvate and lactate, leading
to lactic acidosis.
Causes for Thiamine deficiency
Due to Increased consumption
• Carbohydrate rich diet
• Pregnancy
• Fever
• Hyperthyroidsm
• Lactation
Due to Increased depletion
• Diarrhoea
• Diuretics therapy
• Dialysis
• Hyperemesis gravidarum
Due to decreased absorption
• Chronic gastric inflammation
• Alcoholism
• Malabsorption syndrome
• Gastric bypass surgery
Biochemical features in thiamine
deficiency
• Decreased level of thiamine and carboxylase
TPP in blood and urine.
• Accumulation of pentose sugars in RB cells
due to retardation of transketolation reaction.
• Increased level of pyruvic acid and lactic acid
in blood,due to retardation of oxidative
decarboxylation of pyruvic acid.
Laboratory investigations in thiamine
deficiency
• 24 hrs urinary thiamine
• Transketolase activity
Treatment of thiamine deficiency
• Supplemental thiamine
• Mild neuropathy – 10-20mg/day for 2 weeks.
• Moderate /severe neuropathy – 20-30mg/day
treatment should be continued after few
weeks of disappearance of symptoms.
• In cases of edema and congestion in cardiac
beri beri – 100 mg iv OD.
Prognosis of Beri beri
• Usually good unless in cases progressed to
koroskoff syndrome. In such cases damage is
minimally irreversible.

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Thiamine.pptx

  • 2. THIAMINE (Vitamin B1) • Also called as Antiberiberi factor, antineuritic vitamin. • It is involved in carbohydrate, fat , aminoacid and alcohol metabolism. • Free thiamine is a basic substance and contains (a) a pyrimidine, and (b)a thiazole ring. • It contains sulphur(sulphur containing vitamin).
  • 3. • The active coenzyme form of thiamin, vitamin B1, is thiamin pyrophosphate (TPP) . It is formed by addition of two phosphate groups, by thiamine pyrophosphate transferase.
  • 4.
  • 5. THIAMINE (Vitamin B1) Sources • Aleurone layer of cereals (food grains) is a rich source of thiamine. Therefore, whole wheat flour and unpolished hand pound rice have better nutritive value than completely polished refined foods. • Liver, meat and eggs supply considerable amounts. Ham/pork meats are particularly rich.
  • 6. Biosynthesis : • Synthesized by plants, yeasts and bacteria. • Not synthesized by human beings, hence should be supplied in diet. • Intestinal bacterial flora can synthesize the vitamin. • There can be a substantial loss of thiamine in cooking above 100degrees.
  • 7. Absorption • Free thiamine is absorbed readily from the small intestine. • Bulk of the dietary vegetable thiamine is in the “free” form. In tissues, it is actively phosphorylated to form Thiamine pyrophosphate (TPP) in Liver, and to a lesser extent in other tissues like muscle, brain and RBC Cells.
  • 8. Storage • Capacity to store is limited. • It is present in both free and combined forms in heart (highest concentration), Liver and kidneys. • In lower concentration in skeletal muscle and brain. • Total amount of Thiamine in body is approx. 25 mg.
  • 9. Recommended Daily Allowance of Thiamine • It depends on calorie intake (0.5 mg/1,000 calories). • Requirement is 1.5–2 mg/day. • Actual requirement is related more directly to carbohydrates content of diet than to calorie value of diet.
  • 10. Requirements Increases in • Anoxia-shock and hemorrhage, Serious illness and injury, During prolonged administration of broad-spectrum oral antibiotics, Increased calorie expenditure like fever, hyperthyroidism, Increased carbohydrate intake, Increased alcohol intake, and pregnancy and in lactation.
  • 11. Metabolic Role of Thiamine • Pyruvate dehydrogenase: The coenzyme form is thiamine pyrophosphate (TPP). It is used in oxidative decarboxylation of alpha-keto acids, e.g. pyruvate dehydrogenase catalyzes the breakdown of pyruvate, to acetyl-CoA, and carbon dioxide.
  • 12. • Alpha-ketoglutarate dehydrogenase: requires TPP is the oxidative decarboxylation of alpha- ketoglutarate to succinyl- CoA and CO2. α-ketoglutarate succinyl- CoA + CO2
  • 13. • Transketolase: in the hexose monophosphate shunt pathway of glucose.
  • 14. • B1 is also required in amino acid Tryptophan metabolism for the activity of the enzyme Tryptophan pyrrolase. • Also acts as a coenzyme for mitochondrial branched-chain α-ketoacid decarboxylase which catalyzes oxidative decarboxylations of branched- chain α-ketoacids formed in the catabolism of valine, Leucine and Iso-leucine. • The main role of thiamine (TPP) is in carbohydrate metabolism. So, the requirement of thiamine is increased along with higher intake of carbohydrates
  • 15. Deficiency Manifestations of Thiamine • The deficiency of thiamine produces a condition called beriberi. It is characterized by the following manifestations • CV manifestations: These include palpitation, dyspnea, cardiac hypertrophy and dilatation, which may progress to congestive cardiac failure.
  • 16. • Neurological manifestations: These are predominantly those of ascending, symmetrical, peripheral polyneuritis. • These neurological features may be accompanied occasionally by an acute polyencephalitis which is then called as Wernicke’s encephalopathy. Carl Wernicke in 1894 and Sergiei Sergievich Korsakoff in 1887 described the condition.
  • 17.
  • 18. • Clinical features are those of encephalopathy (ophthalmoplegia, nystagmus, cerebellar ataxia) plus psychosis. It is seen only when the nutritional status is severely affected. • GI symptoms: Amongst these, anorexia is an early symptom. There may be gastric atony, with diminished gastric motility and nausea; fever and vomiting occur in advanced stages.
  • 19. Types of beri beri • Dry beriberi: Central nervous system (CNS) manifestations are the major features. Peripheral neuritis with sensory disturbance leads to complete paralysis. It is not associated with edema. • Wet beriberi: Here cardiovascular manifestations are prominent. Edema of legs, face, trunk and serous cavities are the main features.
  • 20.
  • 21. • Infantile beriberi: It occurs in infants born to mothers suffering from thiamine deficiency. Restlessness and sleeplessness are observed. Absence of deep tendon reflexes. • Thiamine deficiency is manifested as horizontal ridges in nails.
  • 22. • Polyneuritis: It is common in chronic alcoholics. • Alcohol inhibits intestinal absorption of thiamine, leading to thiamine deficiency. • Thiamine deficiency in alcoholism may cause impairment of conversion of pyruvate to acetyl CoA. The result is increased plasma concentration of pyruvate and lactate, leading to lactic acidosis.
  • 23. Causes for Thiamine deficiency Due to Increased consumption • Carbohydrate rich diet • Pregnancy • Fever • Hyperthyroidsm • Lactation
  • 24. Due to Increased depletion • Diarrhoea • Diuretics therapy • Dialysis • Hyperemesis gravidarum
  • 25. Due to decreased absorption • Chronic gastric inflammation • Alcoholism • Malabsorption syndrome • Gastric bypass surgery
  • 26. Biochemical features in thiamine deficiency • Decreased level of thiamine and carboxylase TPP in blood and urine. • Accumulation of pentose sugars in RB cells due to retardation of transketolation reaction. • Increased level of pyruvic acid and lactic acid in blood,due to retardation of oxidative decarboxylation of pyruvic acid.
  • 27. Laboratory investigations in thiamine deficiency • 24 hrs urinary thiamine • Transketolase activity
  • 28. Treatment of thiamine deficiency • Supplemental thiamine • Mild neuropathy – 10-20mg/day for 2 weeks. • Moderate /severe neuropathy – 20-30mg/day treatment should be continued after few weeks of disappearance of symptoms. • In cases of edema and congestion in cardiac beri beri – 100 mg iv OD.
  • 29. Prognosis of Beri beri • Usually good unless in cases progressed to koroskoff syndrome. In such cases damage is minimally irreversible.