Vitamin B12 & Deficiency

VITAMIN B12 (COBALAMIN)

• It is also called as extrinsic factor of castle.
• It contains 4.35% cobalt by weight.
• Corrinoids are cobalt containing weight possessing corrin ring.
• Active form of cobalamin is methylcobalmine and deoxyadenosylcobalamine.
• Coenzyme role of Cobalamine-

a) Isomerisation of methylmalonyl CoA to succinyl CoA-

• methylmalonyl-CoA is accumulated and excreted in urine as methylmalonic acid (methylmalonate) in vitamin B I2 deficieny i.e. methylmalonic aciduria.

b) Conversion of homocystein to methionine-

• Reaction catalyzed by cobalamin-dependent methionine synthase also called 5- methyltetrahydrofolate- homocysteine methyltransferase.

 Vitamin B12 Metabolism–

• It is absorbed in Ileum.
• The internal absorption of Vitamin B12 requires intrinsic factor (IF), secreted by parietal cells of the stomach.

 Transport of Cobalamin to the target tissues-

• Major Cobalamin transport protein in plasma is Transcobalamin II (TC II).

 Sources of Vitamin B12-

• Animal origin only includes meat, eggs, milk and fish.
• Absent in plant foods.
• Synthesized in the intestine by the intestinal flora.

 Vitamin B12 Deficiency-

• Vitamin B12 deficiency is caused due to-

1. Nutritional- strict vegetarians are at a risk.
2. Pernicious anaemia
3. Gastric- congenital absence of intrinsic factor or gastrectomy.
4. Intestinal- intestinal stagnant loop syndrome, Crohn’s disease.
5. Neuropathy- subacute combined degeneration(SCAD), demyelination
6. Fish tapeworm

• Deficiency of Vitamin B12 causes folate trap.

 Clinical Manifestations–

1. Megaloblastic anaemia
2. Homocysteinemia
3. Methyl Malonic Aciduria
4. Subacute Combined degeneration
5. Demyelination
6. Corectal scotoma

•  Daily Requirement dose-

Exam Important

• It is also called as extrinsic factor of castle.
• It contains 4.35% cobalt by weight.
• Corrinoids are cobalt containing weight possessing corrin ring.
• Active form of cobalamin is methylcobalmine and deoxyadenosylcobalamine.
• Coenzyme role of Cobalamine-

a)     Isomerisation of methylmalonyl CoA to succinyl CoA-

• methylmalonyl-CoA is accumulated and excreted in urine as methylmalonic acid (methylmalonate) in vitamin B I2 deficieny i.e. methylmalonic aciduria.

b)    Conversion of homocystein to methionine-

• Reaction catalyzed by cobalamin-dependent methionine synthase also called 5- methyltetrahydrofolate- homocysteine methyltransferase.

 Vitamin B12 Metabolism–

• It is absorbed in Ileum.
• The internal absorption of Vitamin B12 requires intrinsic factor (IF), secreted by parietal cells of the stomach.

 Transport of Cobalamin to the target tissues-

• Major Cobalamin transport protein in plasma is Transcobalamin II (TC II).

 Sources of Vitamin B12-

• Animal origin only includes meat, eggs, milk and fish.
• Absent in plant foods.
• Synthesized in the intestine by the intestinal flora.

 Vitamin B12 Deficiency-

• Vitamin B12 deficiency is caused due to-

1. Nutritional- strict vegetarians are at a risk.
2. Pernicious anaemia
3. Gastric- congenital absence of intrinsic factor or gastrectomy.
4. Intestinal- intestinal stagnant loop syndrome, Crohn’s disease.
5. Neuropathy- subacute combined degeneration(SCAD), demyelination
6. Fish tapeworm 

• Deficiency of Vitamin B12 causes folate trap.

 Clinical Manifestations–

1. Megaloblastic anaemia
2. Homocysteinemia
3. Methyl Malonic Aciduria
4. Subacute Combined degeneration
5. Demyelination