This document discusses fat-soluble vitamins, including their classifications, functions, dietary sources, deficiency signs, and toxicity. Specifically, it details vitamins A, D, E, and K, highlighting their biochemical roles, importance for health, and consequences of deficiency or overdose. It emphasizes the distinct storage and absorption characteristics of fat-soluble vitamins compared to water-soluble vitamins.

1. Fat soluble
Vitamins
Dr. Farhana Atia
Assistant Professor
Department of Biochemistry
Nilphamari Medical College, Bangladesh

2. Classification
Vitamins
Water-soluble
Non-B-Complex
Vit-C
B-Complex
Energy
releasing
Haemato-
poietic
Others
Fat-soluble
Vit-A
Vit-D
Vit-E
Vit-K

3. Fat soluble vitamins
Common
Name
Chemical Name Active Form
Vitamin A
Retinol
Retinal
Retinoic acid
β-carotene
Retinol
Retinal
Retinoic acid
Vitamin D
Cholecalciferol
Ergocalciferol
1, 25
Dihydroxycholecalciferol
Vitamin E α- tocopherol α- tocopherol
Vitamin K
Phylloquinone
Menaquinone
Menadione
Phylloquinone
Menaquinone
Menadione

4. Criteria of Fat Soluble Vitamins
 Soluble in organic or fat solvent (Benzene/ Ether)
 Released, absorbed, transported with fat diet
 Not readily excreted in urine
 Stored in liver & adipose tissue
 Only vitamin K has coenzyme activity
 Have toxic effect if intake is more than RDA (vit A, vit
D)
 Deficiency features develop slowly than water soluble
vitamins.

5. Vitamin A
Pro vitamin A
• carotenoids
• from plants
• Yellow, orange & dark green
vegetables & fruits
• Carrot
• Pumpkins
• Papaya (ripe)
• Mango
Preformed vitamin A
• Retinoids
• from animals
• Liver
• Kidney
• Fish oil
• Egg
• Muscle meat
• Whole milk
• Cream
• Butter

6. Retinoids (Preformed vitamin A)
1. Retinol
 Alcohol
 Storage form of vitamin A
2. Retinal
 Aldehyde derivative of retinol
 Retinol ↔ retinal
3. Retinoic acid
Acid
Retinol Retinoic acid

7.  1 RAE (retinol activity equivalent)
1 μg of retinol
12 μg of β-carotene
3.33 IU (now obsolete)
 β-carotene  cleaved into 2 retinal in intestine but
conversion is inefficient
Adult male 900 RAE
Adult female 700 RAE
RDA

8. Functions of Vitamin A
• Maintain reproduction by supporting
spermatogenesis in male
• prevention of fetal resorption in female.
• Maintain vision by formation of visual
pigment ‘Rhodopsin’ in retina.
• Promotion of growth
• Maintain integrity of epithelial tissue.
Retinol
&
Retinal

9. • Epithelial tissue differentiation &
mucous secretion
• Gene expression
• Promotion of growth
• Have role in cancer prevention
Retinoic
acid
• Antioxidant, so
• prevent cancer & heart disease
β
carotene

10. Rhodopsin cycle
comprises 2
Bleaching of
rhodopsin generate
nerve impulse
Regeneration of
rhodopsin

11. Features
(Vitamin A
deficiency
is the most
important
preventabl
e cause of
blindness)
Loss of sensitivity to green light (earliest sign)
Impairment to adapt dim light
Night blindness
Xerophthalmia (in prolonged deficiency)
Keratinization of cornea
Blindness
Increased susceptibility to infectious disease
Keratinization of skin
Atrophy of epithelium
Growth retardation

12. Hypervitaminosis A
 Excessive intake (not carotene) produce toxic syndrome
(supplement usually, also diet)
 UL: 3000 μg/d
 In pg: teratogenesis (congenital malformation of
developing fetus)
 Symptoms of toxicity affects-
CNS (↑ CSF pressure)
Headache, Nausea, Ataxia,
Anorexia
Calcium homeostasis
Thickening of long bone,
Hypercalcemia, Calcification of
soft tissue
Liver
Hepatomegaly,
Hyperlipidemia
Skin
Excessive dryness, Alopecia,
Desquamation,

13. VITAMIN D
Solar vitamin
In human skin : 7-Dehydrocholesterol, an
intermediate in synthesis of cholesterol
Undergoes a nonenzymatic reaction on
exposure to UVL yielding pre-vitamin D.
Cholecalciferol is formed after further reaction
over a period of hour and absorbed into
bloodstream.
Maximum vitamin synthesis: 10AM – 2PM

14. Dietary Sources
 Required only in individuals
with limited exposure to
sunlight
 Plant- D2/ Ergocalciferol
 Animal- D3/ Cholecalciferol
Fatty fish
Liver
Egg yolk
Milk- after fortification
Cheese
Butter
Child 400 IU
Adult 200- 400 IU
Pg/ Lactation 400 IU
> 60 years 600 IU

15. Formation of Vitamin D
UVL
↓
Skin : 7 DHC → Cholecalciferol (D3)
↓
Liver : 25 hydroxyD3/ calcidiol
↓
Kidney (PCT) : 1, 25 dihydroxyD3/
calcitriol (Active form)
Enz: 25 hydroxycholecalciferol 1
hydroxylase

16. Formation of active vitamin D:
Stimulated by Inhibited by
1. ↓ plasma Ca
2. ↓ plasma PO₄
3. ↑ PTH
4. Estrogen
Prolactin
GH
1. ↑ plasma PO₄
2. ↑ Free ionized plasma
Ca

17. Functions of vitamin D
Maintain adequate plasma Ca level by
 ↑ uptake of Ca by intestine
 Minimize excretion of Ca by kidney
(stimulate reabsorption in distal renal
tubule)
 Stimulate Ca mobilization from bone when
necessary

18. Functions of vitamin D
Regulate gene expression & cell differentiation
 Insulin secretion
 Synthesis & secretion of parathyroid & thyroid
hormones
 Inhibit production of interleukins by activated T-
lymphocytes & immunoglobulin by activated B-
lymphocytes
 Differentiation of monocyte precursor cells
 Modulation of cell proliferation

19. Parathyroid hormone & vitamin D
↓ Plasma Ca
↓
+ PTH
↓
+ 1, 25
dihydroxyvit D
1. ↑ Ca mobilization from bone
2. ↑ Renal reabsorption of Ca
3. ↓ Renal excretion of Ca
4. ↑ Ca absorption from intestine
(1-3 : with the help of PTH)

20. Vitamin D & Ca Homeostasis
Condition GIT Bone Kidney
↓ [Ca]
↑ Ca
absorption
↑ mobilization Active vit D formation
↑ [Ca]
↓ Ca
absorption
[+] Calcitonin
[-] Ca mobilization
↑ excretion (calcitonin)
↓ reabsorption (PTH)
Inactive vit D formation
↓ vit D
No
absorption
[+] Ca mobilization
(PTH)
↓ excretion (PTH)
↑ reabsorption (PTH)
↑ vit D ↑ absorption
↑↑ mobilization
↑ accumulation
↑ excretion (calcitonin)
Inactive vit D formation

21. Deficiency of vitamin D
Rickets
• In children (adolescent also)
• Failure of mineralization of growing bone
Osteomalacia
• In adults (especially women)
• Demineralization of pre-existing bone

22. Rickets
Rickets is the failure in
mineralization of growing
bone or osteoid tissue.
Types
1. Nutritional rickets
 In vitamin D deficiency
 Bones of children are
undermineralized as a result
of poor absorption of Ca
 Treatment: Vitamin D

23. Rickets
2. Renal rickets
In CRF- ↓ Ability to form active vitamin D
Treatment: Active vitamin D
3. Hypophosphatemic rickets (vit D resistant rickets)
Defective tubular reabsorption of PO₄
Treatment: Vit D analog + PO₄
4. Vitamin D dependent rickets
Defective tubular reabsorption of HCO₃⁻, PO₄,
Glucose & AA .
Treatment: High dose of vitamin D

24. Osteomalacia
In adults
Demineralization of preexisting bones
as a result bone soften & osteoporosis occurs.
↑ Susceptibility to fracture.
More incidence- persons in poor daylight
Findings
↓ Serum Ca
↓ Serum PO₄
↑↑ Serum alkaline phosphatase

25. Toxicity of vitamin D
 Most toxic (only in dietary excess, not in excess
exposure to sunlight)
 100,000 IU for wks/ months
 Cl/F
↑ Plasma Ca (↑ absorption & bone resorption)
↑ Deposition of Ca in many organs (artery, kidney)
Calcification of soft tissue
Loss of appetite
Nausea, thirst, stupor
↑ BP

26. VITAMIN E
α-Tocoferol (most active among 8)
Functions:
Antioxidant in prevention of non enzymatic
oxidation of cell component (PUFA) by
molecular oxygen & free radicals.
As an antioxidant it protects erythrocyte
Prevent blood clot associated with heart
block & stroke.

27. Source of vitamin E
Vegetable oil (main)
Grains
Leafy vegetables
Liver
Egg
RDA of vitamin E
Male: 15 IU
Female: 12 IU
High with
increased intake of
PUFA
(polyunsaturated
fatty acid)

28. Deficiency of vitamin E
 Unknown
 Severe fat malabsorption
Cystic fibrosis
CLD
 Premature infant
Born with inadequate reserve
Erythrocyte- abnormally fragile
Hemolytic anemia
Toxicity: Least toxic

29. Vitamin K
Phyloquinone
Biologically active
Source – Green vegetables
Menaquinone
Intestinal flora
Synthetic
Menadiol
Menadion
Menadiol diacetate

30. Diet
 Cabbage
 Cauliflower
 Spinach
 Broccoli
 Egg yolk
 Cheese
 Liver
Intestinal flora- In ileum.
RDA
Male 70- 80 IU
Female 55- 65 IU

31. Function of vitamin K
Hepatic synthesis of prothrombin
Activation of coagulation factor (II, VII, IX, X) by
γ-carboxylation of glutamic acid residue.
Precursor of
factor II, VII, IX
,X
CO₂ Warfarin
Mature
clotting
factors
O₂ Vit K

32. Deficiency of vitamin K
True deficiency is unusual
(Bacterial flora)
Steatorrhea
Administration of broad
spectrum antibiotic (alter
intestinal bacterial flora → ↓
synthesis of vit K)
Deficiency feature
Bleeding tendency
Prolong PT
Large dose &
prolong
administration
 Hemolytic anaemia
 Jaundice (due to
toxic effect on RBC
membrane)
Toxicity

33. Newborn has less vitamin K
Very little can be transported across the placenta
Sterile intestine
Protein synthesis has not yet reach full adult
capacity particularly in premature infant
Deficiency is severe enough to cause
hemorrhagic disease of newborn (2- 3 days of
birth)
Treatment- Single I/M inj. of Vitamin K as
prophylaxis

34. Thank You