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