Vitamin B Complex Part I PDF

NDT2123 Principles of Human Nutrition Vitamin B Complex PART 1 Ms Farah Yasmin binti Hasbullah [email protected] Division of Nutrition a...

NDT2123 Principles of Human Nutrition Vitamin B Complex PART 1 Ms Farah Yasmin binti Hasbullah [email protected] Division of Nutrition and Dietetics Inspire Empower Elevate Copyright (C) 2024. School of Health Sciences. IMU University. For internal circulation in IMU University ONLY.  Lesson outcomes 1. Identify chemical structure of vitamin B-complex 2. State the requirement of vitamin B-complex for human 3. State and discuss its basic functions of vitamin B- complex in human metabolism 4. State and describe the symptoms of the deficiency and toxicity of vitamin B-complex 5. Recall and discuss the sources of vitamin B- complex in food 6. Explain the method used for determination of vitamin B-complex 2  Introduction ▪ All vitamin B-complex are water-soluble vitamins o Not stored in body in significant amounts o Some stored in liver in small amounts o Depleted quickly from body o Excreted through urine o Thus, require daily repletion 3  Vitamin B-complex B1 Thiamine The B2 Riboflavin Really B3 Niacin Naughty B5 Pantothenic acid Panda B6 Pyridoxine Prefers B9 Folate Fresh B12 Cobalamin Carrots! 4 Thiamine VITAMIN B1 5 Thiamine 6 Background ▪ First isolated & characterised in the 1920s ▪ One of the first organic compounds to be recognised as a vitamin ▪ One of the first nutrients studied in Malaya – beginning of 20th century ▪ Java, Indonesia: Eijkman observed chicken fed on rice bran not affected by beri-beri ◦ milling removed the important substance from rice ◦ Beriberi became rampant when germ and bran are removed to produce white rice Thiamine Chemical structure Hydroxymethyl group Pyrimidine ring Thiazole ring Methyl group Methylene bridge 7 Thiamine Digestion ▪ From plants: thiamine found as free thiamine ▪ From animal products: as various phosphorylated forms: o Thiamine monophosphate (TMP) o Thiamine triphosphate (TTP) o Thiamine pyrophosphate (TPP), also known as Thiamine diphosphate ▪ Free thiamine: no enzymatic breakdown, ready to be absorbed in small intestine ▪ Phosphorylated forms: intestinal phosphatases hydrolyze the phosphates prior to absorption 8 Thiamine Absorption ▪ Absorption occurs in the jejunum and ileum of intestine o in small amount: Thiamine is absorbed by sodium-dependent active transport mechanism o in large amount: absorption is through passive diffusion ▪ Half of the body’s thiamine is within muscle tissue 9 Thiamine Absorption ▪ Thiamine is rapidly converted into its biologically active form, thiamine pyrophosphate (TPP) in the brain & liver ▪ Synthesis of TPP from thiamine requires Mg, adenosine triphosphate (ATP) & enzyme thiamine pyrophosphokinase 10 Thiamine Functions ▪ Thiamine is involved in numerous body functions: o nervous system & muscle functioning o flow of electrolytes in & out of nerve and muscle cells o multiple enzyme processes (via the coenzyme Thiamine pyrophosphate) o CHO metabolism 11 Thiamine Functions ❑ Thiamine is the vitamin part of the coenzyme thiamine pyrophosphate (TPP) – a required coenzyme for energy metabolism o After glycolysis - Carboxylation of pyruvate to form acetyl- coenzyme A (acetyl-coA) that enters the citric acid cycle o Citric acid cycle - α-ketoglutarate dehydrogenase catalyzed reactions, decarboxylation of α-ketoglutarate to succinyl coA o Pentose phosphate pathway – as coenzyme for the very important protein, transketolase enzyme 12 Thiamine 13 Thiamine Dietary sources ▪ Beef, legumes (beans, lentils), milk, pork, nuts, oats, oranges ▪ Rice, seeds, wheat, whole grain cereals and yeast, enriched white rice with thiamine ▪ Most thiamine is lost during production of white flour & polished (milled) rice ▪ White rice & foods made from white flour (e.g. bread & pasta) are enriched with thiamine in many Western countries ▪ Breads (white) in Malaysia are also fortified with vitamins and mineral 14 Thiamine 15 Thiamine Requirement ▪ Humans are dependent on dietary intake for thiamine ▪ There is very little thiamine stored in the body ▪ Depletion occurs as quickly as within 14 days ▪ RNI: 1.1 – 1.2 mg/day, proportional to caloric intake of the diet ▪ If CHO content is excessive, thiamine intake needs to be increased 16 Thiamine Deficiency ▪ Leads to a severely reduced capacity of cells to generate energy – a result of its role in the pathways ▪ Beriberi – severe Thiamine deficiency, described in Chinese literature (in early 2600 B.C.) ▪ affects the cardiovascular, nervous, muscular & GI systems ▪ 3 types: ▪ dry (wasting) ▪ wet (oedematous) ▪ cerebral – depending on the systems affected 17 Thiamine 1. Dry beriberi ▪ Reflects damage to nervous system ▪ Main feature is peripheral neuropathy ▪ “Burning feet syndrome” may occur in the early course ▪ Other symptoms: o abnormal (exaggerated) reflexes o diminished sensation o weakness in legs & arms o seizures 18 Thiamine 2. Wet beriberi ▪ In addition to neurologic symptoms, it is characterized by cardiovascular manifestations which includes: o rapid heart rate o enlargement of the heart o severe swelling (oedema) o difficulty breathing o congestive heart failure 19 Thiamine 3. Cerebral beriberi ▪ Wernicke’s encephalopathy & Korsakoff syndrome are different conditions result from severe thiamine deficiency i. Wernicke’s encephalopathy o Acute/short-term condition o Affects CNS – mental confusion, motor issues, amnesic symptom not necessarily present ii. Wernicke-Korsakoff syndrome (WKS) o Untreated Wernicke’s often leads to WKS o Amnesic symptoms are present o Most sufferers are alcoholics, those with gross malnutrition, including stomach cancer & AIDS sufferers 20 Thiamine 21 Thiamine Deficiency ❑ Causes of thiamine deficiency: i. Inadequate intake o common in low income populations whose diet is high in CHO but low in thiamine e.g. polished rice o alcoholism is associated with low intake in industrialized countries ii. Increased requirement/ excessive loss from the body o strenuous physical exertion, fever, pregnancy, breastfeeding, growth 22 Thiamine Deficiency ▪ Causes of thiamine deficiency: i. Consumption of anti-thiamine factors (ATF) in food - tea, coffee (including decaffeinated), chewing tea leaves & betel nuts ii. Combination of all the above factors 23 Thiamine Determination of status ▪ Thiamine is a coenzyme needed for transketolase ? ▪ Transketolase decreases early in thiamine deficiency ▪ Thus, measurement of transketolase activity in red blood cells is used to assess the nutritional status of thiamine ▪ This enzyme requires TPP o with a decline in TPP, there is a decline of transketolase activity o results reflect a decrease in dietary intake before any other signs of thiamine deficiency becomes detectable 24 Riboflavin VITAMIN B2 25 Riboflavin Background ▪ Appears as yellow crystal in pure state ▪ Stable against heat, oxidation and acid ▪ Sensitive to alkali & destroyed in the presence of UV light (70% within 4 hours exposure) 26 Riboflavin Chemical structure ▪ Riboflavin is a flavinin which the flavin ring is attached to a Ribitol sugar called ribitol drawn in an open chain conformation Isoallaxone ring 27 Riboflavin Digestion Occurs in food in various Digestion forms: Riboflavin bound to protein HCL, enzymatic hydrolysis of protein FMN (Flavinmononucleotide) FMN phosphatase FAD (Flavinadenine FAD pyrophosphatase dinucleotide) Riboflavin phosphate Intestinal phosphatases 28 Riboflavin ▪ Riboflavin coenzymes 1. FMN: Flavinmononucleotide (structure in black with 1 phosphate group) 2. FAD: Flavinadenine dinucleotide (blue structure in an adenosine monophosphate (AMP) group 29 Riboflavin Absorption ▪ During low to moderate intake: active or facilitated transport ▪ During high intake: passive absorption ▪ More riboflavin is absorbed when taken with meal ▪ Transported by a protein carrier in the blood ▪ Small amount stored in liver and excess is excreted 30 Riboflavin Functions ▪ Precursor for coenzymes flavinmononucleotide (FMN) and flavinadenine dinucleotide (FAD) ▪ Also as a component of FMN and FAD ▪ Required in reactions that extract energy from glucose, fatty acids & amino acids ▪ Supports antioxidant activity of glutathione peroxidase where presence of selenium is required 31 Riboflavin Functions ▪ Coenzymes o functions as H carriers in the mitochondrial electron transport system o also coenzymes of dehydrogenase, which catalyse the first step in oxidation of several intermediates in glucose metabolism & of fatty acids o FMN is required for conversion of phosphorylated pyridoxine (vitamin B6) to its functional coenzyme o FAD for the conversion of tryptophan to niacin 32 Riboflavin Dietary sources ▪ Riboflavin in small amounts is widely distributed in foods ▪ Best sources are: o Milk (fresh, canned or dried/powdered) & milk products e.g. cheddar cheese, cottage cheese o Enriched grains o Liver o Oyster ▪ 60% of vitamin is lost when flour is milled o most breads and cereals are enriched with riboflavin ▪ Sensitive to UV radiation – milk stored in paper, opaque plastic containers 33 Riboflavin Requirement ▪ RNI for adults o Men: 1.3 mg/day o Women: 1.1 mg/day ▪ Recommendation is calculated based on the amount of recommendation for energy intake 34 Riboflavin Deficiency ▪ Rare in developed countries – due to presence in adequate amounts in eggs, milk, meat & cereals ▪ Often seem in chronic alcoholism due to poor dietary habits ▪ Can lead to growth retardation due to inability of several metabolism to proceed ▪ Deficiencies are usually in combination with other water -soluble vitamins 35 Riboflavin Symptoms of deficiency Itching & burning eyes, Ariboflavinosisis – which become sensitive to characterised by development of cheilosis (fissuring of lips), angular light (photophobia) stomatitis (cracks in the skin atthe corner of mouth), purple swollen tongue (glossitis) Cracks & sores at the corner Digestive disturbances of mouth & lips Bloodshot eyes Emotional changes i.e. depression & hypochondria Dry & flaky skin Sore, red tongue Retarded growth Skin rash 36 Riboflavin Determination of status ▪ The status is determined by measuring the increase in activity coefficient of the enzyme glutathione reductase (EGR) in red blood cells (must be fresh, lysed & measured promptly) o FAD is required for EGR activity ▪ Results are expressed as activity coefficient (EGRAC), the ratio of activities in the presence of added FAD & w/o its addition o guidelines for interpretation: EGRAC 1.2 = acceptable; 1.2 – 1.4 = low; > 1.4 = deficient (McCormick & Greene 1994) 37 Niacin VITAMIN B3 38 Niacin 39 Niacin 40 Niacin (Nicotinamide adenine dinucleotide) (Nicotinamide adenine dinucleotide phosphate) 41 Niacin 42 Niacin 43 Niacin 44 Niacin 45 Niacin 46 Niacin ? Question: What is the coenzyme required to convert tryptophan to niacin? 47 Niacin 48 Niacin 49 Niacin Requirement 50 Niacin 51 Niacin 52 Niacin 53 Niacin 54 Niacin 55 Niacin 56 Niacin Determination of status ▪ Most sensitive and reliable measure of niacin status – urinary excretion of 2 major metabolites: ▪ N1-methyl-nicotinamide ▪ N1-methyl2-pyridine-5-carboxamide ▪ High excretion rate – adequate status 57