Water Soluble Vitamins !

C & C & B-complexB-complex VitaminsVitamins

Tapeshwar Yadav(Lecturer)B.M.L.T, D.N.H.EM.Sc. Medical Biochemistry

Tapeshwar yadav.(Lecturer)

B.M.L.T, D.N.H.EM.Sc. Medical Biochemistry

Water soluble vitamins

VITAMINS• “VITAMIN” means “vital for life”

• VITAMINS are *Micronutrients* which are necessary for everyday healthy

functioning of the body.

* Nutrients required in very small amounts - mg or µg

VITAMINS - Two main categories

Water solubleC&

B-complex

Fat SolubleAD E&K

Water v/s Fat Soluble Vitamins

Water v/s Fat Soluble Vitamins

WATER SOLUBLE VITAMINS

Vitamins C & B-Complex • Chemistry &

Properties.• Sources.•Functions.• Deficiency.• RDA .

Water Soluble Vitamins: Characteristics

• Essential • Organic Structure• Non-energy Producing• Micronutrients• Stability • Bioavailability• Toxicity

ASCORBIC ACID (VITAMIN-C)

Anti scorbutic factor, Hexuronic acid.

Chemistry :- White, Crystaline, Odourless with acid taste.

Highly water soluble in Nature.

Empirical formula=C6H8O6.

Structural formula Resembles that of Carbohydrate.

Acidic Properties, due to Enolic Hydroxy groups.

L-Ascorbic acid undergoes oxidation to form dehydro ascorbic acid.

Both are biologically active.

D-Form is inactive.

Oxidation of vitamin-c is rapid in presence of Copper.

Sources :- Amla(Indian Goose Berry)700mg/100g. Guava :- 300 mg/100 G. Green leafy vegetebles.

Absorption :- From intestine not stored in Body.

Ratio of Ascorbic/Dehydro Ascorbic acid is 15 :1 in many tissues.

On hydration Dehydroascorbic acid is converted to oxalate (via) DiketoGulonic acid.

Functions :- Metabolisms Enzymes1) Collagen Hydroxylation of Lysine/Proline. (Hydroxylase)

2) Tyrosine a) P-HPP Hydroxylase. b) Homogentisate oxidase c) Dopamine βHydroxylase.

3) Bile Acid 7-α-Hydroxylase.

4) Folic Acid Formation of FH4

(Folate reductase)5) Tryptophan Tryptophan

hydroxylase

6) Biological Oxidation Cytochrome oxidase

7) Bone formation vitamin-C play important role.

8) Iron Absorption Fe3+ Fe2+

9) Meth-hemoglobin Hemoglobin.

10) Antioxidant property spare the vitamins-A and E.

11) Prevents formation of cataract.

12) Reduces risk of Coronary heart diseases and cancer.

13) Vitamin-C enhances synthesis of immunoglobulins and increased Phagocytic action.

• Deficiency :- Scurvy.• Infants 6-12 months, due to weaning from milk-

dietary defect.

• Infantile scurvy Barlow’s Disease.

Symptoms :- Adults :-• Hypochromic, microcytic anemia.

• Easy fracture of bones.

• Loosing of teeth.

• Poor wound healing.

Deficiency test :-• Sphygmomanometer cuff is placed on the fore

arm, inflated and pressure kept for 5 minutes.

• Petechiae is observed under skin.

• May be rough and dry, pigmented due to abnormality of Tyrosine metabolism.

• Load test :-• Give 500mg of vitamins-C orally.

• Check urinary- vitamin-C level after 5 hours.

• Load test :-• Normal people 100mgs appear in urine.

• Moderate deficiency <20 mg.

• Severe deficiency <5mg.

• RDA :- • 70 mg for normal people.

• >100 mg in case of Pregnancy & Lactation.

Thiamin• Anti Beri-Beri or anti neuritic vitamin.

• Chemistry :- Pyrimidine ring and thiazole ring are held by a Methylene bridge.

Chemistry :-

PYROPHOSPHATE

Sources:-Thiamin mainly concentrated in outer layers of

cereals and breakfast cereals.Oat meal.Wheat germ. Fortified white flour.Unpolished hand pound rice.Vegetables. MilkEggs, Meat.

Sources

Thiamin Sources

• Absorption:• In duodenum.

• Active transport (low Thiamin levels).

• Passive transport (high B1 levels).

Oxidative Decarboxylation Reactions

1) Pyruvate dehydrogenase

Pyruvate+ CoASH + NAD+ TPP Acetyl CoA + CO2

+ NADH+H+

Biochemical FunctionsBiochemical Functions

Oxidative Decarboxyation Reactions

2) α-Keto-Glutarate Dehydrogenase

α KG + CoASH+ NAD+ TPP Succinyl CoA + CO2+NADH+H+

Important in CHO/energy metabolism.

Biochemical FunctionsBiochemical Functions

2) Transketolase :- (HMP-Pathway)

Ribose-5-(P) Sedoheptulose-7-(P) + +

Xylulose-5-(P) Transketolase Glyceraldehyde-3(P) + TPP-Mg+2 +

Erythrose-4-(P) Fructose-6-(P)

RBC transketolase activity is a measure of Thiamin deficiency.

• Oxidative decarboxylation of branched chain amino acids by α- keto acid dehydrogenase.

• TPP or Thiamin triphosphate help in nerve impulse transmission by ion translocation or synthesis of Acetylcholine.

Deficiency of Thiamin :- Beri-Beri-from dutch Eastindies.

• Heaviness of legs, Anoxia, Dyspegia, subjects feel weak.

Beri-Beri

Wet Beri-Beri Dry Beri-Beri Infantile Beri-Beri

Wet Beri Beri• CVS manifestations.• Edema of legs, Face,

Trunk..• Calf muscles are

tender.• Heart becomes weak

failure

Dry Beri-Beri• CNS symptoms.• Muscles progressively

weak.• Peripheral neuritis

paralysis.

• Infantile Beri-Beri :-• Restlessness. • Sleeplessness.• Acute cardiac failure.

• Wernicke-Korsakoff syndrome :-• Cerebral Beri-Beri-Mainly due to nutrition

deficiency.• Encephalopathy-Nystagmus, cerebellar ataxia.• Affinity of TPP towards transketolase.

• Alcoholic Polyneuritis:- Observed in chronic alcoholics.

Polyneuritis Motor and Sensory defects

Old age and Pregnancy thiamin deficiency.

• RDA:- 1.0-1.5 mg.

• Explanations for deficiency symptoms:-

• Pyruvate x Acetyl CoA.

Lactate dehydrogenase Lactate

• Pyruvate, Lactate levels rise in blood, tissues and urine in BERI-BERI causing vasodilatation edema.

• Branched- chain α-ketoacids rise in blood and urine in BERI-BERI as TPP is coenzyme.

• Decline in transketolase activity in BERI-BERI, elevates Pentose levels in blood, urine . Estimation of erythrocyte transketolase activity has a diagnostic value for B1 activity.

• Energy production from glucose is depressed in nerve tissue and heart in BERI-BERI,leading to neuronal inflammations, leisons,lassitude and cardiac failure.

• Neurological symptoms are due to decline in Beri-Beri may be due to decline direct role of TPP in nerve impulse transmission.

Riboflavin = B2• First vitamin among B-complex group to

be isolated in a pure state.

• Vitamin is synthesized by all green plants and most of the micro-organisms.

• Lactoflavin-Milk, Hepatoflavin-liver, Ovoflavin-Egg, Verdoflavin-Grass are chemically identical to Riboflavin.

• Warburg-isolated yellow enzyme is essential for cellular respiration.

• Coloured heat stable pigment decomposes in the presence of visible light.

Chemistry

Riboflavin

Isoalloxazine

Ribitol

+

Riboflavin Flavokinase Flavin mono nucleotide(FMN) ATP ADP ATP Synthase PPi Falvin adenine dinucleotide (FAD)

Chief functions in the body:- Part of coenzymes-

• FAD (Flavin adenine dinucleotide).• FMN (Flavin mononucleotide) used in energy

metabolisms.

• FAD dependent reactions :-1). Succinate dehydrogenase (SDH) :- Succinate Fumarate. FAD FADH2

2). Acyl CoA dehydrogenase:-Acyl CoA α-β Unsaturated Acyl CoA. FAD FADH2

• FAD dependent reactions :-3). Xanthine oxidase :- Xanthine Uric acid FAD FADH2

• FMN dependent :- L-Amino acid oxidaseL-Aminoacid α-Keto acid + NH3 FMN FMNH2

Sources of Riboflavin

Sources :-• Milk/products• Enriched grains• Liver• Oyster• Yeast• Whole grains

• Riboflavin deficiency :-• Its rare, occur with other vitamin deficiencies.• Cheilosis A disorder of the lips often due to

riboflavin deficiency and other B-complex vitamin deficiencies and characterized by fissures, especially in the corners of the mouth

• Inflammation at angles of mouth – Angular stomatitis.

• Lingual papillae atrophy and magenta colored tongue - Glossitis

• Seborrhic dermatitis:- inflammation of sebaceous glands of skin.

Glossitis

Angular Stomatitis

Cheilosis

• Assay :- a) RBC content of Riboflavin. b) RBC glutathione Reductase activity.

• RDA :- 1.5 mg

Niacin Other names1. Vitamin B3.2. Nicotinic acid.3. Nicotinamide.4. Niacinamide.5. Pellagra preventing factor of Gold Berger.

COOH

Pyridine Nicotinic acid (Niacin)

CO-NH2

Nicotinamide

Sources :-• All protein foods.(rich in

Tryptophan)• 60 mg TRP= 1mg Niacin • Milk, eggs, meat, fish, poultry.

• Enriched grains and Nuts.

Sources

Quinolinate QPRT

Chief functions:-– Theraputic uses :- Nicotinic acid for

lowering the plasma cholesterol.– The main coenzymes are two they are 1) NAD+ and 2) NADP+.– NAD+ (Nicotinamide adenine dinucleotide)

and NADP+ (its phosphate form) used in oxidation-reduction reactions of various metabolisms.

• Primary function of coenzymes is to remove hydrogen from substrates.

• AH2 + NAD+ NADH + H+ + A

Hydrogen ion

• NAD+ Reactive site is carbon atom 4 and NADP+ nitrogen atom of Nicotinamide ring.

• Rest of the molecule binds to apoenzyme.• Oxidized form Reduced form NAD+ NADH + H+

NADP+ NADPH + H+

• These coenzymes participate in the oxidation and reduction series of reactions.

• NAD+ dependent reactions Glycolysis :- a) Glyceraldehyde-3-phosphate dehydrogenase. b) Lactate dehydrogenase.

TCA cycle :- a) Pyruvate dehydrogenase. b) Isocitrate dehydrogenase. c) α-Ketoglutarate dehydrogenase. d) Malate dehydrogenase.

• NAD+ dependent reactions• Aminoacid catabolism :- a) Branched chain α-Ketoacid dehydrogenase b) Glutamate dehydrogenase• Fat metabolism ;- a) β-Hydroxy acyl CoA dehydrogenase b) β-Hydroxy butyrate dehydrogenase

NADP+ dependentGlucose Dehydrogenase.Isocitratedehydrogenase.Glucose-6-Phosphatase.Malic enzyme.

NADPH dependent• Dihydro folate reductase.• Phenylalanine hydroxylase.• Met Hb reductase.• Cholesterol -7-a hydrolase.• Squalene epoxidase.• HMG- CoA reductase.

• 3-Keto acyl CoA reductase.• Glutathione reductase.• Glucose 6-(P) dehydrogenase.• 6-Phospho gluconate dehydrogenase.

DeficiencyPellagra(3D’s disease):-1.Dermatitis.2.Diarrhea.3.Dementia.

Dermatitis• Inflammation of skin.• Red, itchy, dry thickened, pigmented skin in

hands, feet, axila, wrist, and knees.

Dermatitis of Pellagra

Diarrhea: Abnormal, frequent evacuation of watery feces.

• Intestinal leisons• Vomiting.

Dementia• Delerium – Impairement of

memory.• With cerebral, spinal lesions,

irritability and anxiety.

Cause of deficiency :- • Maize rich diet where Niacin is in bound,

not useful.• Sorghum rich diet Leucine inhibits

Quinolinate Phoshoribosyl transferase.

RDA :- - 13-19 mg . 13x 60 mg to 19x60 mg .• Tryptophan (60mg) Pyridoxal phosphate (PLP).

Niacin (1mg).

Toxicity symptoms– Painful flush, hives, and rash (Niacin flush)– Excessive sweating– Blurred vision– Liver damage, impaired glucose tolerance.

Thank you !

Pyridoxine = B6• Other forms of this vitamin.

– Vitamin B6.

– Pyridoxal.– Pyridoxal phosphate.– Pyridoxamine.

Pyridine

CH2OH

CHO CH2-NH2

CH2OHCH2OH

HO CH2OH

H3C

H3C

HO HO

H3C

Pyridoxine

Pyridoxal Pyridoxamine

CHOCH2O-PHO

H3C

Pyridoxal phosphate

CHOOH

CH3

CH2OH

+ ATP + ADP

Pyridoxal

Absorption :- All forms of B6 are absorbed from intestine.

Pyridoxal + ATP Pyridoxal phosphate+ADP Kinase (Major)

Pyridoxamine +ATP Pyridoxamine phosphate+ADP (Minor)

4-Pyridoxic acid (End product)

Functons :-Part of coenzymes PLP (pyridoxal phosphate) and PMP (pyridoxamine phosphate) used in amino acid and fatty acid metabolism.Transamination reaction (transaminase).Aspartate+αKG ASTOxaloacetate+Glutamate

Alanine+αKG ALTPyruvate+Glutamate

Heme biosynthesis (ALA synthase). Carbohydrate metabolism . PLP is a part of muscle phosphorylase

(Glycogenolysis). Lipid metabolism-Formation of sphingo lipids

and myelin sheath. Neurotransmitter Synthesis. 5-Hydroxy Tryptophan Serotonin Conversion of tryptophan to niacin.

Decarboxylation of amino acid (decarboxylase).Glutamate GABAHistidine Histamine

• Dietary sources• Rice polishing, Wheat germ,• Milled Cereals, pulses, oil seeds.• Milk, Meat, fish, Poultry, Liver.• Potatoes, Legumes, Soya products

and green leafy vegetables.

Dietary Sources

• Deficiency :- Severe B6 deficiency is characterized by

increased excretion of xanthurenic acid in urine. Tryptophan

3- OH Kynurenine

PLP X Xanthurenic acid excreted in urine3-OH Anthranilate Quinolinate QPRT NMN

NAD+ and NADP+

• Deficiency :- Neurological symptoms are present since

biological amine synthesis is decreased. Mental confusion, Irritability, Nervousness,

Depression.

Hypochromic Microcytic anemia due to decreased synthesis of Hb.

De-myelination of nerves lead to peripheral neuritis.

Commonly observed during lactation and alcoholism.

RDA :- Daily Value set at 2 mg• 1.3 mg for adults• 1.7 mg for men over 50• 1.5 mg for women over 50• Average intake is more than the RDA

Folate• Other names

– Folic acid– Folacin– Pteroyl glutamic acid (PGA).

Chemistry:- Pteridine ring - PABA - glutamate.

9 10

• Stability :-– Very sensitive to heat.– Easily oxidized.– Leached.

Absorption

Metabolism

Dietary Sources:-• Fortified Grains• Leafy Green Vegetables• Legumes, Seeds• Liver

Dietary Sources

Functions Folic acid NADPH+H+ NADP+ Folate reductase DihydrofolateNADPH+H+ NADP+ Dihydrofolatereductase

Tetrahydrofolate

THF mainly functions as a carrier for one carbon groups.

The one carbon group may be carried on N5 or N10 or both of tetrahydrofolate.

They are Methyl(-CH3), Methylene(=CH2) Methenyl(=CH-), Formyl(-CH=O), Fomimino (-CH=NH).

All one carbon groups are inter convertible. -CHO +H2 -CH2OH -H2 -CHO

Sources of one carbon groups :- Serine is the major source. Other sources are Glycine, Tryptophan &

Histidine.

• Fate of one carbon groups :-• N5, N10 methylene THF provides methylene

group to :a) Uracil to form thymine. Thymine is important for

DNA synthesis.b) Glycine to form serine.

• N5 methyl THF provides the methyl group to Homocysteine to form methionine. This reaction needs cobalamin.

• N5, N10 methenyl THF provides C8 of Purine ring.

• N5 formyl THF provides C2 of Purine ring.• Purines are components of nucleic acids.

• N5-formyl tetrahydrofolate is also called Citrovoram factor folinic acid, is used as a supplement to folic acid, more effective than folic acid in anti-cancer treatment.

Factors causing folate deficiency :-1) During pregnancy.2) Defective absorption a) Sprue b) Coeliac disease3) Resection of jejunum.4) Anticonvulsant drugs will inhibit intestinal

enzyme– Folate absorption decreases5) During excessive hemolytic reaction.

Deficiency manifestations :-Intracellular concentration of Tetrahydrofolate.

No conversion dUMP dTMP

No DNA synthesis.

No cell division

• Macrocytic Anemia :-• Hb accumulates in RBC precursors.• Reticulosis :- Abnormal RBC trapped in spleen

and destroyed, leads to decreased RBC life span

• Peripheral smear :- Macrocytic type.• Daily 300-500 µg of folate will improve the

blood picture in the first condition.

Pancytopenia all blood cells are affected. Leucopenia decreased WBC. Thrombocytopenia decreased platelets. Impaired growth.

• Neural Tube Defects

– Malformation of the central nervous system that forms very early in the pregnancy (often even before woman realizes she is pregnant.

• Spina bifida- Spine develops outside of the body.

• Anencephaly- Entire brain and skull above the ears is missing.

Neural tube defects Spina Bifida Anencephaly

Folacin • Only known way to prevent these congenital

malformations is adequate Folacin intake prior to pregnancy

• Adequate folic acid intake can reduce the risk of Neural tube defects by up to 75%.

• Assessment of Folate deficiency :-1). Normal serum folate = 20 ng /ml.2). Histidine load : 2-15g. (FIGLU excretion) test :- Histidine -----> Formiminoglutamic acid-

X Excreted in urine

Glutamate3). Peripheral blood picture.

THF

Formyl THF

Antagonists:-a) Trimethoprim.b) Sulphonamides.c) Aminopterin.

• RDA:- 100 μg

Vitamin B12

• Synonyms :- Cobalamin. Extrinsic factor of castle. Antipernicious anemia factor.

Chemistry :- 4 Pyrrole ring co-ordinated with cobalt atom is called as corrin ring.

4-Pyrroles substituted + Cobalt

Corrin ring Dimethyl benzimidazole + Ribose-5 (P)+ Amino isopropanol

Cobalamin

AbsorptionIt requires

– HCl– Pepsin– Intrinsic factor

Diet Vitamin B12 attached to proteins

Stomach Proteolytic enzymes Proteins B12 intrinsic factor of castle

GP (Molecular weight 50,000)Complex of Intrinsic factor and B12

NOTE:- GP=Glycoprotein secreted by Gastric perietal cells

• Intrinsic factor-B12 complex passes on ileum of gut, where it is absorbed.

• Binding of complex and entry of B12 into mucosal is mediated by calcium ions .

Plasma10% TC-II

B12 Mucosal cell Methyl B12 90% Trans cobalamin-I TC-I-B12

Other tissues TC-II-B12

Methyl B12 Deoxyadenosyl B12

• TC-I B12 Only water soluble vitamin stored in body about 2 mg in liver which is useful till 2-3 years

Sources• Animal products

– Meat, poultry fish, shellfish.– Milk, cheese.– Eggs.– Not present in the vegetables.– Intestinal micro organisms synthesize B12 in

human colon but it is not absorbed through the mucosa.

Sources

• Coenzymes:-• Vitamin B12 exists in two coenzyme forms.1) Methyl cobalamin2) 5’-deoxy adenosyl cobalamin.

Coenzymes of vitamin B12 :- Cobalamin + Methyl tetrahydo folate

in Cytoplasm

Methyl-cobalamin + Tetrahydro folate.

Functions :-Participates in Methionine biosynthesis:- Homocysteine + N5 Methyl tetrahydrofolate Methyl transferase Methylcobalamin Methionine + Tetrahydrofolate(important for haemopoiesis)

Methionine is a Lipotropic factor which prevents the fatty liver.

• Methionine is an important factor for the formation of phospho lipids, later found in the structure of myelin sheath.

• Isomerism of L-Methyl melonyl coA Succinyl coA by methyl melonyl coA mutase with the help of 5’deoxy adenosylcobalamin in odd chain fatty acids metabolism.

• In some bacteria :- Cobalamin derivatives useful for Ribose Deoxyribose

DNA synthesis

• Deficiency :-• Decreased vitamin B12 intake, this may occur

among vegetarians.• Atrophy of gastric mucosa lack of intrinsic

factor, this give rise to a condition Pernicious anemia above 60 years of age.

• Pernicious anemia :- Low Hb levels, decreased number of erythrocytes.

• Auto antibodies against gastric parietal cells.• Anti bodies against intrinsic factors.• Defctive absorption as in Sprue or regional

enteritis.• Drugs induced vitamin B12 deficiency. Anticonvulsants, Phenformin, Neomycin,

Cholestyramine, Para-aminosalycylic acid.

• Deficiency manifestations :-• B12 deficiency

N5 Methyl THF No formation of THF• This condition is called folate trap or • Methyl trap Decreased folate co-enzymes

Reduced nucleotide and DNA synthesis Megaloblastic anemia.

• Megaloblastic anemia is a macrocytic hypochromic anemia.

Neurological manifestations :- It is due to lack of myelin sheath due to deficiency of methionine and disturbance in the metabolism of odd chain fatty acids.

It includes sub-acute combined degeneration of spinal cord :-

Sensory and Motor tracts are effected. Paresthesia of extremities. Alterations of reflexes. Loss of memory. Peripheral neuritis leads numbness, tingling and

weakness of extremities.

Treatment :- Megaloblastic anemia can be treated with folate alone.

But lesions cannot improved. So 100-1000µg of B12 is given intramuscularly.

• Assessment of B12 deficiency :- B12 serum – Radio immuno assay (RIA). increased methyl malonic acid excretion in urine

(i.e Methylmalonic aciduria). Peripheral blood and bone-marrow morphology. Check for Achylia gastrica.

Biotin• Synonyms :- Vitamin-H. Vitamin B7.• Anti egg white injury factor.

Sources• Widespread in foods both Animal and

Plant origin.• Liver, Kidney, Fish, Egg yolks, Milk.• Tomatoes, Soybeans, Whole grains.

Sources

• Storage :-• After absorption, Biotin is stored in liver as

Biocytin (Biotinyl-5-Adenylate)• Biotin functions as a component of multi-subunit

enzymes that catalyze carboxylation reactions.

Multi-enzyme complex :-• Biotin carrier protein.• Biotin carboxylase.• Biotin acyl transcarboxylase.

Enzyme Pathway Reaction catalyzed

Propionyl CoA Carboxylase

Amino acids-1).Valine, Isoleucine, Threonine.2). Odd chain fatty acid metabolisms.

Propionyl CoA

Methyl melonyl CoA

Acetyl CoA Carboxylase

Fatty acid synthesis

Acetyl CoA

Malonyl CoA

β-Methyl crotonyl CoA carboxylase

Leucine catabolism

β-Methyl crotonyl COA

β-Methyl glutaryl CoA

Deficiency :-• The deficiency occurs in sulfonamide treatment

also, causes destruction of intestinal flora.• Deficiency of holocarboxylase synthetase in

children. The enzyme responsible for attachment of biotin for carboxylase enzyme.

• Deficiency symptoms :-1)Retarded growth2)Dermatitis3)Alopecia4)Loss of muscular control.5)Immuno deficiency disease.

Avidin :-• Raw egg white – contains Avidin- Glycoprotein

had high affinity to Biotin.• Intake of raw egg white (un-boiled) may cause

Biotin deficiency-(20 Raw eggs/day for prolonged time).

• Avidin is heat labile, boiling of egg will neutralize inhibitory activity.

Leiner’s disease :-• Occurs in breast fed young infants with

persistent diarrhoea.

• Low Biotin in human milk leads to deficiency.

Antagonist :- Desthiobiotin.

RDA :- 200-300 μg.

Pantothenic Acid• Greek word “Panto” means everywhere or

Universal.

• It is known as chick anti dermatitis factor.

Chemistry :- Pantoic acid + β-Alanine

Pantothenic acid

Sources• Widespread in foods.• Organ meats.• Mushrooms.• Avocado.• Broccoli.• Whole grains.

Sources

Functions :-Coenzyme A (CoA SH):- Synthesized from

cysteine, Pantothenic acid, AMP and phosphate.

Functions of Coenzyme A :- It has a terminal thiol group (-SH).

• Thiol group act as carrier of acyl or acetyl and succinate group.

Biochemical Role

Carbohydrates

Pyruvate Acetyl CoA

Alanine Leucine Glucogenic Ketogenic aminoacids

Fatty acid Acetyl Choline Cholesterol TCA cycle Ketone bodies Detoxification

α-Ketoglutarate Suyccinyl coA Gluconeogenesis Activation of aceto acetate

ODD chain Fatty acids Porphyrins Energy Threonine, Valine, Isoleucine Drug metabolism

Deficiency :- • Rare in humans. However “burning feet syndrome”

soldiers of second world war- Paresthesia in lower extremities, staggering gait.

• Sleeplessness :- Linked to this vitamin deficiency.• This syndrome observed in prison camps,• Chronic alcoholic famine, renal dialysis patients.

• RDA:- 5-10 mg

Actions of the B Vitamins

• Non-B Vitamins • Controversial other dietary compounds• Still under scientific investigation• May be “conditionally” essential• Supplements NOT necessary• Widespread in foods.

• Choline(Trimethyl hydroxy ethanolamine):-• It is needed in relatively big amount.• Adequate Intake for Men=550 mg/day; Women=425 mg/day• Formed from serine.

Functions:-• Participates in the formation of lecithin and

sphingomylein.• Lipotropic action (prevents the fatty liver)• Helps in the formation of acetyl Choline.• Involved in the one carbon metabolism due to

the presence of three methyl groups.• By oxidation it is converted into Betaine.

• Inositol(Hexahydroxy cyclohexane):- • Also called as myoinositol or mesoinositol.• It is sugar alcohol derived from glucose.• Lipotropic factor.• It is a component of phospholipid, phosphatidyl

inositol-Part of cell membrane structure.• Acts as a second messenger for some hormones.

Lipoic acid(6,8 dithio octanoic acid):-• Sulphur containing fatty acid.• Fat as well as water soluble.• Exist in oxidized and reduced form.• As an antioxidant it reduces free radicals.• Reduces the insulin resistance.

Biochemical functions :-• Decarboxylation reactions• Pyruvate PDH Acetyl coA• Keto glutarate SDH Succinyl coA

• Vitamin Imposters• Ubiquinone (Coenzyme Q10)• Orotic acid.• Lipoic acid.• Vitamin O (oxygenated salt water)• Vitamin B15 (Pangamic acid)• Vitamin B17 (Laetrile)

Conclusions 1. Vitamins are derived from a variety of

foods. That is why variety is so important.2. Vitamin deficiencies rarely occur.3. If they do, it is usually in conjunction with

severe illness, stress, or trauma that is superimposed on prolonged inadequate intake.

4. If there is deficiency, usually several vitamins (especially in the case of B vitamins) are involved.

5. Toxicity is also rare but a possibility– Toxicity is rarely associated with food– Toxicity results from supplements

6. Vitamin imposters are used

Variety is the Key

Vitamins are

derived from

a variety of

foods.

THANQ

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