Micronutrients 2

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B vitamins

Water soluble vitamins
Group of organic micronutrients with very different structures but common area of function
Coenzymes- almost all coenzymes include B vitamins
Participate in all metabolic pathways- can't have metabolic processes without them
Needed by all cells- not a big difference between plant cells, microbial cells and animal cells
Deficiency symptoms often very general with some specific
Essential for all cells, including bacteria
Bacterial synthesis in the gut can contribute to requirements
In ruminants synthesis is anterior to absorption so ruminants are largely independent of a dietary source of B vitamins
In humans bacterial synthesis posterior to most absorption so contribution not as high and greater need for dietary source

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B vitamins in Metabolism

Thaimin
Riboflavin
Niacin
Biotin
Pyridoxine
Panrothenate
Folate
B12

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Thiamin B1

Part of coenzyme thiamin pyrophosphate (TPP)
Involved in pentose phosphate pathway and conversion of pyruvste to acetyl CoA
Fundamental to energy metabolism- fundamental for conserving carbohydrate energy in form of lipid as if eat too much carb stored as lipid but goes through this reaction first
U.K. Requirements set relative to energy intake
RNI- 0.3-0.4 mg thiamin/1000 calories

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Thiamin Deficiency Symptoms

Develops when most of energy from carbohydrate (polished rice) (tend to develop when high amount of energy comes from carbphydrate)
Wernicke-Korsakov syndrome in alcoholism
Tiredness, irrationality, depression
Beri-beri- dry- peripheral neuropathy (tingling limbs, numbness, paralysis); wet- odema, cardiac dysfunction, death

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Riboflavin B2

Part of coenzymes flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN)
Involved in TCA cycle, b-oxidation, conversion of pyruvate to acetyl CoA

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Riboflavin Deficiency Symptoms

Cracks around mouth
Inflammation of lips/tongue
Skin lesions around nose, genetalia
Anaemia

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Niacin (nicotinic acid, nicotinamide)

Part of nicotinamide adenine dinucleotide coenzymes NAD+ and NADP+
NAD+ involved in energy generation from glycolysis, TCA cycle, B-oxidation and conversion of pyruvate to acetyl CoA
NADP+ involved in synthetic reactions e.g malonyl pathway
Can be synthesised from tryptophan
NAD us usually involved in oxidation reactions which are generating energy so gets reduced and feeds into ETC
NADP picks up hydrogens to use in synthetic reactions
Usually require dietary source to ensure there's enough
Number of things we see happening to epithelial cells on skin are also happening to epithelial cells on the gut

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Niacin Deficiency Symptoms

Pellagra- cracking skin, de-squamation, hyperkeratosis, skin hyperpigmentation, diahorrea, dementia, delirium

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Biotin

Prosthetic group of carboxylase enzymes (enzymes which are catching CO2 and adding an extra carbon to molecules) e.g pyruvate carboxylase- used when pyruvate converted to oxaloacetate during gluconeogenesis (ability to synthesise glucose from compounds which can be used to synthesise pyruvate depends on biotin) and acetyl CoA carboxylase- enzyme at beginning of malonyl pathway (converts acetyl CoA to malonyl CoA and is fundamental to synthesis of FA) more involved in synthetic reactions because fixing carbon
Involved in gluconeogenesis and FA synthesis

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Biotin Deficiency Symptoms

Unlikely
No known deficiency in adults; dermatitis, alopecia, ketosis can occur in infants (biotin involved in synthesis of OA, needed for TCA)- if can't make enough OA to keep TCA going then end up with ketosis

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Biotin Antagonist

Avidin (in raw egg whites) acts as antagonist
Binds to biotin and prevents absorption in normal way
-deficiency often not through intake but through antagonist

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Pyridoxine (pyridoxal, pyridoxamine) B6

Pyridoxal phosphate involved in AA metabolism- transfers NH2 group
Involved in deamination (picks up NH2 from AA and takes it away) and transamination (where it's eventually converted to ammonia or picks it up from one AA and puts it on a ketoacid to mKe new AA)

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Pyridoxine Deficiency Symptoms

Very rare
Irritability, depression, loss of sense of responsibility
Convulsions
Raised plasma homocysteine concentration

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Cobalamin B12 (requires cobalt in its structure (c

Very complex molecule
Found as adenosyl cobalamin (picks up adenosyl group) or methylcobalamin (picks up a methyl group), acts as carrier of 1C units
Involved in conversion of propionyl CoA to succinyl CoA (in order to be metabolised first has to be converted to CoA derivative then goes through series of reactions which convert it to succinyl CoA (medium in TCA) if don't have B12 propionyl CoA doesn't get into central metabolic pathway- get odd number of FA in ruminants)'and homocysteine to methionine
Requires presence of intrinsic factor (binds to B12, cells in gut recognise it and then absorb both by endocytosis) produced in parietal cells of the stomach, to enable absorption in the ileum
Transcobalamin helps transport B12 in blood, sometimes get B12 deficiencies in ruminants because don't have enough cobalt to make B12

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Cobalamin Deficiency Symptoms

Dietary deficiency rare except in strict vegans (B12 more widely distributed in animal tissues than plant tissues)
Symptoms due to absorption failure: pernicious anaemia (enlarged, immature red blood cells), demyelination of nerves
Raised plasma homocysteine concentrations

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Folic acid

Similar but separate function to B12- folic acid gets hydrogenated, pick up 2H or 4H
Exists in di- and tetra-hydrofolate forms; acts as carrier of 1C units
Involved in
-AA metabolism (homocysteine to methionine)
-purine metabolism (C2 and C8 of A and G)
-nucleotide synthesis (dUMP to dTMP) (d-deoxy)- uracil not a base usually found in DNA, in RNA U replaces T- important for DNA synthesis- if not enough TMP to make new DNA, either won't make it or will put in UMP which isn't correct

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Folic Acid Deficiency Symptoms

Megoblastic anaemia (enlarged immature blood cells)
Raised plasma homocysteine concentration
Risk factor for development of neural tube defects (NTD)- actual link not proven but link between low folate concentration and development of NTD proven time and time again
Some symptoms shared with B12 (homocysteine concentration and megoblastic anaemia) and B6 (raised homocysteine concentration)

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Pantothenic Acid

Part of CoA and acyl carrier protein (ACP)- central to metabolism
Involved in FA synthesis, b-oxidation, link between glycolysis and TCA cycle, activation of acyl groups

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Pantothenic Acid Deficiency Symptoms

Very rare
'Burning foot' syndrome
Abdominal pain
Nausea
Weakness
Cramps
Insomnia
Alopecia

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Iron

Component of haem in haemoglobin and myoglobin, component of cytochromes, cofactors for some enzymes e.g aconitase
Stored in liver and other cells e.g enterocytes bound to protein ferritin
Exists in Fe2+ and Fe3+ forms- important for functions, can induce free radical formation
Mainly present in diet as Fe3+ (feric) 67% or as haem iron 33%- non-vegetarians
Vitamin C reduces it to Fe2+ in gut lumen- can only be absorbed as Fe2+ so need mechanisms to convert Fe3+ to Fe2+
Vegetarians reliant on inorganic iron
Shape makes it active aconitase and it participates in TCA cycle- if not enough iron in body, protein can't bind around iron atom and so has different shape- in that shape will bind to RNA of whole range of proteins that are associated with iron metabolism- when not enough iron present it acts as an iron regulatory protein, when there is enough it binds round it, acts as aconitase and generates energy
Ability for ferus iron to convert to feric iron and release electron is quite a damaging reaction to cell

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Dietary Iron Absoprtion

Present in plasma, bound to protein called transferrin
Unique as no excretory method for iron- very careful control of absorption

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Iron Deficiency and toxicity Symptoms

4th most abundant nutrient on earth but most common nutritional deficiency
Iron deficiency anaemia (reduced peak cell volume and Hb concentration)
Impaired immunity
Impaired mental and motor development in early life
Reduced energy, lethargic, reduced capacity for work

Toxicity- siderosis and organ damage (in excess)

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Iodine

Component of thyroid hormones T3 (tri-iodothyronine) and T4 (thyroxine)
Iodisation of salt programmes

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Iodine Deficiency Symptoms

Goitre, cretinism if foetus suffers from deficiency- mental retardation, deaf mute, squint, disorders of posture
Thyroid gland produces thyroid hormones- can only do this if have enough iodine present- if don't thyroid produces message sating need more thyroid hormones so enlarges to produce more but still can't as doesn't have enough iodine so gets bigger- increase size to increase capacity- neck swells, if happens during pregnancy affects development of brain in infants

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Salt Iodisation

Addition of iodine to salt intended for human and animal consumption
Cost effective and viable solution to prevent iodine deficiency disorders
Iodine content of iodised salt UK is recommended to be 10-22mg/kg salt (through addition of potassium iodide)
Iodised salt for discretionary domestic use, although once readily available to buy in UK isn't so now, few manufacturers world wide use it in preparation of manufactured goods
Currently no mandatory iodine supplementation of salt or other food UK

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