Water Soluble Vitamins in a Nutshell

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water soluble vitamins

Water Soluble Vitamins in a Nutshell

Vitamins are broadly classified as Water soluble and Fat Soluble. Water soluble vitamins are B Complex and C. They are usually not stored in the body even if taken in excess quantities. B Complex vitamins act as coenzymes for various enzyme.

The following is a summary of the functions and deficiency manifestations of water soluble vitamins.

Name Biochemical name Active (Coenzyme) form Required for the activity of Deficiency disease
B1 Thiamine Thiamine Pyro Phosphate (TPP)
  1. PDH
  2. α ketoglutarate dehydrogense
  3. Branched chain α keto acid dehydrogenase
  4. Transketolase
B2 Riboflavin Flavin Mono Nucleotide (FMN)Flavin Adenine Dinucleotide (FAD) NADH dehydrogenase, amino acid oxidaseAcyl CoA dehydrogenase etc Angular stomatitis, Glossitis, Cheilosis
B3 Niacin Nicotinamide Adenine Dinucleotide (NAD),Nicotinamide Adenine Dinucleotide Phosphate (NADP) **** Pellagra
B5 Pantothenic acid CoA,Acyl carrier protein Gopalan’s burning foot syndrome
B6 Pyridoxine Pyridoxal phosphate (PLP) ****
Biotin Biotin Coenzyme for carboxylases ****
Foilc acid TetraHydroFolic Acid (THFA) One carbon group transfer Megaloblastic anemia
B12 Cobalamin Methyl CobalaminDeoxy adenosyl cobalamin HS-Met methyl transferaseMethyl malonyl CoA mutase Megaloblastic anemiaPernicious anemia


Additional Points to remember


Deficiency is common in alcoholics and those who consume polished rice

The 4 enzymes (see chart) that require TPP do not function

Leads to Beriberi


  • 2 types- dry beriberi and wet beribery
  • DRY BERIBERY: PDH is inhibited; So glucose metabolism interrupted; Nervous tissue affected; leads to neuropathy and extreme tiredness. (Beriberi = extreme tiredness)
  • WET BERIBERI: PDH inhibited, pyruvate accumulates and gets converted to lactate; Lactate causes cardiac failure.
  • Earliest biochemical manifestation in beriberi:- Decreased transketolase activity in RBC


Active forms NAD and NADP; they act as coenzymes for various dehydrogenases

NAD requiring enzymes Eg:

Betahydroxy acyl CoA dehydrogenase

Isocitrate dehydrogenase

Malate dehydrogenase

(They convert NAD to NADH which is equivalent to 2.5 ATP)

NADP requiring enzymes (NADPH producing enzymes) Eg:

Mainly enzymes of HMP shunt

Glucose-6-phosphate dehydrogenase

6-phosphogluconate dehydrogenase

NADPH requiring enzymes

All reductases in biosynthetic pathways (Eg: HMG CoA reductase)

Niacin can be synthesized in the body from Tryptophan. (60 mg of Trp can form 1 mg niacin)

2 enzymes are important in the conversion of trp to niacin

  1. Kynureninase : This requires PLP as coenzyme (So any condition causing PLP deficiency will also cause Pellagra)
  2. QPRTase: Rate limiting enzyme in the pathway. Inhibited by Leucine. (So high dietary leucine will cause pellagra)

Causes of Pellagra

Nutritional Causes

  1. Dietary deficiency
  2. People whose staple diet is maize. (Maize contains niacin in a bound, unabsorbable form “niacytin”)
  3. Pyridoxine deficiency (Because Kynureninase requires PLP)
  4. Leucine pellagra: People who eat Sorghum (Guinea corn) as staple diet: Sorghum has high Leucine content. This inhibits QPRTase

Non-nutritional causes

  1. INH therapy: INH is an antituberculous drug. This inhibits pyridoxal kinase and inhibits the formation of PLP.
  2. Hartnup disease: Absorption of Trp is defective. Trp deficiency leads to niacin deficiency
  3. Carcinoid syndrome: All the available trp is converted to serotonin

Clinical features

3D: Diarrhoea, Dementia, Dermatitis

Diarrhoea with blood in stools; leads to loss of weight

Dermatitis: severe in exposed areas of skin. “Casal’s necklace”

Dementia: Loss of memory



Active form: PLP

PLP requiring enzymes:


ALA synthase

Aminoacid decarboxylases

Glycogen phosphorylase

Cystathionine beta synthase




Coenzyme for carboxylases (So, known as co-carboxylase)

Biotin deficiency occurs in those who consume raw eggs; Egg white contains a heat labile glycoprotein called “Avidin” which binds biotin tightly and prevent its absorption



Active form is THFA; it is a carrier of one carbon units

Folic acid is Pteroyl glutamic acid. Formed from Pteridine and PABA. Converted to THFA by folate reductase

Foalte antagonists

Sulphonamides: have structural similarity with PABA. So they inhibit folate synthase in bacteria. They are given as antibacterial drugs

Methotrexate: Has structural similarity with Folic acid; inhibit folate reductase. Used as anticancer drug


Cobalamin (B12)

Has Corrin ring (Tetrapyrrole ring with cobalt at its centre)

Major circulating form is methyl cobalamin

Major storage form is deoxyadenosyl cobalamin (AdoB12)


Causes of deficiency

  • True veg
  • Gastrectomy, gastric atrophy, chronic iron deficiency
  • Pernicious anemia
  • Pregnancy
  • Fish tapeworm


Absorption of B12 requires Intrinsic factor of Castle. Deficiency of Intrinsic factor causes B12 deficiency and leads to anemia; this is called pernicious anemia

Other features of B12 deficiency are SACD (Subacute combined degeneration), Methyl malonic aciduria etc

Schilling test is done to assess B12 absorption


Vitamin C (Ascorbic acid)

Bleeding Gums in Scurvy

Bleeding Gums in Scurvy

Heat labile vitamin; Present abundantly in citrus fruits and amla

Has reducing property

Functions of vitamin C

  1. Maturation of collagen; Hydroxylation of proline and lysine requires vitamin C
  2. Absorption of iron: Iron is kept in ferrous form by vitamin C
  3. Other enzymes that require vitamin C are:
    1. Trp hydroxylase
    2. Dopamine β oxidase
    3. Folate reductase
    4. 7 α hydroxylase
  4. Antioxidant–> reduce the risk of cancer

Deficiency –> Scurvy (Sailor’s disease)

Mainly due to absence of fresh fruits and veg from diet

Bleeding gums, hypochromic anemia etc.

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