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NUTR2101 > Water Soluble Vitamins > Flashcards

Water Soluble Vitamins Flashcards

1
Q

List all the water soluble vitamins, their coenzyme form and distinct features

A

B1- Thiamin - Thiamin pyrophosphate
Present food as free thiamine (plant), or thiamine pyrophosphate (TPP)
Transport by RBC
Converted in liver
Bioavailability lowers by thiaminases and thiamin oxidases
RDI, no UL
Beriberi and Wernicke-Korsakoff

B2- Riboflavin - Flavin adenine dinucleotide or flavin mononucleotide
Converted in tissues
Excess in urine = bright yellow
RDI, no UL
Light exposure = breakdown
Angular stomatas, scale skin

B3 - Niacin - Nicatinamide adenine dinucleotide or Nicatinamide adenine dinucleotide phosphate
Bioavailability low in grain
Endogenous synthesis from tryptophan
Activation in tissues
RDI (niacin equiv.), UL (supplements and fortified foods)
Pellagra and 4Ds

B5 - Pantothenic Acid - Coenzyme A
Present as panto and coA in food. Must be freed
Transport bound to RBC
Deficiency rare
AI, no UL
Headaches, burning feet fatigue

B6 - Pyroxidine - Pyridoxal phosphate
Found in food as PLP, must be converted for absorption
Passive diffusion
Activated in liver
RDI, UL
Microcytic hypochromic anemia, oily dermatitis

B7 - Biotin - Biologically active as biotin
Found in food as biotin or biotinyl (bound to lysine), must be freed
Active transport
AI, no UL
Skin rash, patchy hair loss, impaired growth

B9 - Folate/folic acid - Tetrahydrofolate/ tetrahydrofolic acid
Synthetic form more potent
Polyglutamates must be broken down to monoglutamated by folate conjugase for active transport
Folic acid passive diffusion
Activation in enterocytes (folate) and liver (folic acid)
Circulates in many forms
Signifiant storage in liver (500-2000ug)
RDI as Dietary Folate Equivalent to account for both food sources, UL for folic acid
Megaloblastic (macrocytic) anaemia, spina bifida
Can mask B12 deficiency since same type of anaemia

B12 - Cobalamin - Methyl cobalamin, 5-deoxy-adenosyl-cobalamin
Synthesised by bacteria
Bound to protein in food, released by HCL and pepsin
Absorbed in terminal ileum via endocytosis
Storage in liver ~2500ug
RDI, no UL
Magaloblastic/macrocytic anaemia, severe nerve degeneration (loss of myelin sheath)

Choline
Can be synthesised in liver
Does not function as coenzyme
Oxidised in liver as betaine
AI and UL
Vitamin C - ascorbic acid
AA = active transport
DHA = facillitated difffusion
RDI, UL
Scurvy in deficiency
Kidney stones in excess
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2
Q

What is the difference between cofactors and coenzymes? Which are B vitamins

A

Coenzyme: usually when the prosthetic group of an enzyme is an organic compound

Cofactors: usually when the prosthetic group of an enzyme is a metal ion

Most B vitamins active only as coenzymes

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3
Q

What are the general features of water soluble vitamins?

A

Storage: overall minimal, but there are exceptions

Toxicity: risk of toxicity/adverse effect is less than for fat-soluble vitamins, but can occur for some vitamins

Water soluble vitamins can be damaged or reduced in concentration during food preparation/cooking, when exposed to heat, light, oxygen and alkaline substances

Thiamine is removed in the process of polishing rice
“Parboiled” white rice (soaking, steaming, and drying in the husks) contains 80% of the thiamine of brown rice

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4
Q

Describe the digestion, absorption, transport, storage and excretion of thiamine

A

Digestion-absorption:

- Small intestine, active or passive absorption
- Present in food as free thiamine (plant), or thiamine pyrophosphate (TPP) in animal products, HCl is required to free TPP from protein foods
- Only free thiamine is absorbed: intestinal phosphatases de-phosphate TPP back to thiamine for absorption
- Conversion of free thiamine to coenzyme TPP in liver

Transport: by RBC to tissues as TPP

Storage: minor amount stored in muscles and the liver

Excretion: excess rapidly filtered by kidneys and excreted via urine

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5
Q

Describe the functions of thiamine?

A

Functions as TPP only

  1. Assists enzymes involved in CHO and BCAA metabolism (clears toxic byproducts of transamination)
  2. Thiamine is needed for normal function of the nervous system
  3. Required in decarboxylation reactions
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6
Q

Describe the signs and symptoms of thiamine deficiency

A
  1. Beriberi
    • Dry Beriberi: nervous and muscular system malfunction
    • Wet Beriberi: nervous and muscular system + CVS malfunction
  2. Wernicke-Korsakoff syndrome: cerebral beriberi in alcoholism
    • Reduced thiamine absorption due to alcohol reducing expression of thiamine transporters in the enterocytes
    • Increased thiamine excretion with excess alcohol consumption
    • Leads to cortical damage: double vision, crossed eyes, ataxia, constant shake, memory loss, impaired mental function

No UL so no toxicity

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7
Q

What is the reason for mandatory thiamine fortification?

A

Thiamine deficiency from alcohol abuse was the “reason” for mandatory fortification of thiamine in bread flour, and voluntary fortification of cereal-based foods in Australia

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8
Q

What are some foods that lower the bioavailability of thiamine?

A

Raw fish contain thiaminases

Brussel sprouts and beets contain thiamin oxidants

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9
Q

Describe the digestion, absorption, transport, storage and excretion of riboflavin

A

Digestion-absorption:

- HCl in stomach releases riboflavin bound to dietary compounds
- Free riboflavin absorbed via active transport or diffusion depending on concentration
- Only 60-65% of intake is absorbed

Transport:

- Transported by protein carriers in the blood
- Converted to the coenzyme forms (FAD or FMN) in most tissues

Storage: small amount stored in liver, kidneys, heart

Excretion: excess excreted in urine and will cause bright yellow urine when taken as a supplement

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10
Q

Describe the 6 functions of riboflavin

A
  1. Key roles in energy metabolism in the CAC + ETC: FAD and FMN shuttle H atoms into the ETC
  2. FAD required in the CAC
  3. In beta-oxidation: conversion of FA to acetyl coA requires fatty-acyl dehydrogenase, which required FAD
  4. The reduction of glutathione (part of endogenous non-enzymatic antioxidant system) requires the activity of a FAD-dependent enzyme: glutathione reductase
  5. The formation of niacin (B3) from tryptophan (AA) requires FAD
  6. Formation of the vitamin B6 coenzyme form (PLP) requires FMN
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11
Q

Describe the signs and symptoms of riboflavin deficiency

A

Signs/symptoms: glossitis, angular stomatitis (pictures), scaly skin, anaemia, fatigue, headaches

RBC, riboflavin and glutathione reductase concentrations indicate riboflavin status (biomarkers)

Increased risk: chronic alcoholism, malabsorption syndromes, use of contraceptive pill, high stress, elderlies

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12
Q

What are some good food sources of riboflavin

A

Dairy milk products

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13
Q

What are the requirements for riboflavin?

A

RDI, no UL

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14
Q

Describe the digestion, absorption, transport, storage and excretion of niacin

A

Digestion-absorption
- Niacin bioavailability is low in grain, especially corn: tightly bound to protein; less than 30% can be absorbed
§ Soaking corn in lime water can improve bioavailability. This method is used where corn is a staple food
- Most absorption in the small intestine: active transport and passive diffusion depending on concentration available
- Endogenous synthesis can occur with tryptophan as precursor (only endogenous water-soluble vitamin)

Transport and activation: converted to coenzyme form in all tissues: NAD+ and NADP+

Storage: limited storage in liver

Excretion: excess excreted in urine

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15
Q

What molecules does niacin encompass?

A

nicotinic acid, nicotinaminde, nicotinamide riboside

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16
Q

What are the signs and symptoms of niacin deficiency?

A

Pellagra = rough skin

4 Ds = Dermatitis, diarrhoea, dementia, death

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17
Q

What are the requirements of niacin?

A

RDI as niacin equivalents since it can by synthesised from tryptophan

60mg tryptophan = 1mg niacin

UL applies to supplements and fortified foods only. Based on observed flushing reactions due to peripheral vasodilation

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18
Q

Describe the digestion, absorption, transport, storage and excretion of pantothenic acid

A

Digestion-absorption:
Present in food as free pantothenic acid and 85% as coenzyme A (CoA)
Released from coenzyme A by digestion in SI
Active transport and passive diffusion depending on concentration available
Only 40-60% of intake is bioavailable

Coenzyme form: CoA forms when pantothenic acid combines with a derivative of ADP and the AA cysteine in any cells requiring it. (note: CoA is not acetyl-CoA, but is part of it, when it combines to acetate)

Transport: bound to RBCs and transported around the body freely

Storage: minimal storage, but present in every cell of the body as CoA

Excretion: excess excreted in urine

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19
Q

What are the primary functions of pantothenic acid?

A

Essential as CoA for the formation of acetyl CoA in all energy production pathways

Acetyl CoA is the building block in the synthesis of cholesterol, FA, steroid hormones, bile acids

Pantothenic acid is part of acyl-carrier proteins; shuttle FA through the pathway of FA elongation: adding of carbon atoms in lipogenesis

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20
Q

Describe the requirements of pantothenic acid

A

AI, no UL

Deficiency is rare because it is found in a large variety of foods

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21
Q

What are the characteristic signs and symptoms of pantothenic acid deficiency?

A

Headaches, burning feet fatigue, impaired muscle coordination, GIT disturbances

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22
Q

Describe the digestion, absorption, transport, storage and excretion of pyroxidine

A

Digestion-absorption

- Present in food in the coenzyme form pyridoxal phosphate (PLP). Converted to B6 for absorption. The animal source form is more readily absorbed 
- Passive diffusion in small intestine
- Can also be absorbed in the coenzyme form if a lot is available

Transport

- Portal vein to liver
- Active form PLP made in the liver, circulates in blood to tissue bound to albumin

Storage: muscle tissue is the main storage site

Excretion: excess excreted in urine

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23
Q

What are the primary functions of PLP?

A
  1. Involved in many enzymatic reactions, especially involving nitrogen groups
  2. Required in almost all AA metabolism and transamination
  3. Required in glycogenolysis: maintaining blood glucose levels during short-term fasting
  4. Required in the synthesis of key metabolic compounds:
    • Haem ring
    • Histamine
    • Neurotransmitters
    • Production of niacin from tryptophan
  5. Gene expression regulation
  6. Modulation of effects of steroid hormones
    Involved in immune function regulation
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24
Q

Describe the requirements of B6

A

RDI and UL

25
Q

What are the signs and symptoms of B6 deficiency? Who is at risk?

A

Oily dermatitis

Microcytic hypo-chromic anaemia (small and pale) due to reduced heme and haemoglobin synthesis

At risk with very poor diet, malabsorption issues, chronic alcoholism (acetaldehyde blocks PLP formation in liver)

26
Q

What is a good food source of B6?

A

Oatmeal

27
Q

Describe the digestion, absorption, transport, storage and excretion of biotin?

A

Digestion-absorption

- Found in food as free biotin or biocytin (bound to the AA lysine in protein)
- Biotinidase unbinds biotin from lysine for absorption
- Free biotin absorbed by active transport
- Bioavailability greater in eggs and meat sources
- Some minor microbial production in large intestine
- Generally biologically active as biotin (exception to the coenzyme rule)

Storage: minimally stored in liver, muscle, brain

Excretion: mainly via urine, some in bile

28
Q

Describe the primary functions of biotin

A
  1. Required in carboxylation reactions
  2. Required for metabolism of CHO, fats and proteins, and formation of CAC intermediates
  3. Catabolism of BCAAs: ketogenic BCAA to make acetyl-CoA
  4. Involved in DNA folding in the nucleus
  5. Involved in the production of oxaloacetate from pyruvate
29
Q

What are the requirements for biotin?

A

AI, no UL

30
Q

Describe the signs and symptoms of deficiency and possible causes

A

Symptoms include skin rash, patchy hair loss, impaired growth

May be due to biotinidase deficiency or excessive raw egg white consumption (avidin in egg whites inhibits biotin absorption in the SI)

31
Q

What are some food sources of biotin?

A

Chicken liver, chicken nuggets, peanuts

32
Q

What does the term “folate” describe?

A

A general term for two types of food sources: folate (natural food sources) and folic acid (synthetic form used in fortified foods and supplements)

Folate in natural foods is 50-80% bioavailable compared to folic acid (which is 100% bioavailable due to increased stability)

Folate can contain multiple glutamates
Folic acid contains one glutamate = optimal absorption

33
Q

Describe the digestion, absorption, transport, storage and excretion of folate

A

Digestion-absorption:

- Food processing destroys 50-90% of folate (heat, oxidation, light)
- Polyglutamate must be broken down in the GIT to monoglutamates by folate conjugase for absorption (zinc dependent)
- Folate monoglutamate: absorbed by active transport in small intestine
- Folic acid (supplements and in fortified food): passive diffusion
- Coenzyme = tetrahydrofolate/ tetrahydro folic acid (THF/THFA)

Activation:
- Conversion to coenzyme occurs in the enterocytes for folate and in the liver for folic acid by dihydrofolate reductase

Transport

- Circulates in many forms: the main form is 5-methyl THFA (5 Me-THFA)
- Converted back to polyglutamates in cells (traps folate inside cells)

Storage: significant amount stored in the liver (about 500-2000ug, equal to several months supply) => one of the exceptions for water soluble vitamins

Excretion: via urine and faeces

34
Q

Describe the functions of folate

A

Central role as coenzyme THFA: cell division, proliferation, and maintenance of new cells

  1. DNA synthesis and repair
  2. Formation of serotonin, adrenalin, dopamine
  3. Amino acid metabolism: in transamination
  4. Conversion of homocysteine to methionine in collaboration with vitamin B12
  5. THFA is “recycled” by vitamin B12 (importance discussed later)
35
Q

What are the requirements of folat?

A

RDI expressed as dietary folate equivalent to account for both sources in diet

1ug dietary folate equivalent = 1ug natural folate = 0.5ug folic acid on empty stomach = 0.6ug folic acid with meals

UL for folic acid

36
Q

Describe the characteristic signs and symptoms of folate deficiency

A

DNA synthesis and repair impaired: affects especially the rapidly dividing cells (e.g. RBC and GIT cells)
§ => in bone marrow, precursor cells (WBC and RBC) cannot form new DNA => causes formation of large immature RBC (less cells overall too) = megaloblastic (or macrocytic) anaemia: fatigue, weakness, shortness of breath
§ => in GIT: poor absorption of nutrients, as GIT cells are poorly renewed or formed => diarrhoea, deficiency of micronutrients

37
Q

Describe the effect of folate in pregnancy

A
  • Deficiency of folate peri-conception (before and after conception) and during early stages of pregnancy = increased risk of neural tube defect in unborn child; e.g. Spina bifida
    § CSF doesn’t flow properly, pressure builds up in brain, ventricles expand
38
Q

What are the common causes of folate deficiency?

A
  • Poor absorption (i.e. due to polymorphism in folate conjugase: less polyglutamate to monoglutamate conversion => less absorption)
  • Alcoholism: alcohol interferes with folate conjugase
  • Polymorphism in dihydro folate reductase (conversion to active THFA)
  • Vitamin B12 deficiency (needed to “recycle” THFA)
    Methotrexate (anti cancer-recurrence medication0 is a folate antagonist to reduce the proliferation of cancer cells; but also impacts healthy cells
39
Q

Describe the characteristic signs and symptoms of folate toxicity

A

Increased carcinogenesis because of DNA damage

Adverse reproductive and developmental effects

May mask vitamin B12 deficiency: B12 deficiency leads to the same type of anaemia, but B12 deficiency comes also with severe permanent neurological damage if not addressed

40
Q

How is cobalamin synthesised?

A

Exclusively by bacteria (even industrially) due to its complex structure

41
Q

What are the synthetic and natural forms of B12?

A

Synthetic form = cyanocobalamin

Natural form = cobalamin

42
Q

Describe the digestion, absorption, transport, storage and excretion of cobalamin

A

Digestion-absorption:

- Cobalamin bound to protein in food 
- Released by action of HCl and pepsin in stomach
- Free cobalamin binds to R-protein in the stomach (produced by salivary cells + parietal cells)
- In small intestine, pancreatic protease release cobalamin from R-protein
- Free cobalamin binds to intrinsic factor (IF) (produced by parietal cells)
- IF + B12 travel to, and are absorbed at, the terminal ileum by endocytosis via cubilin. Cellular uptake via endocytosis
- Absorption is increased with increased intake
- Small amount also absorbed by passive diffusion

Transport: taken to the liver and body cells bound to trans-cobalamin proteins 1, 2 and 3

Storage: liver, enough for 2-3 years: ~2500ug (another exception in water soluble vitamins)

Excretion: very little in urine, some excretion via bile, but most is recycled via enterohepatic circulation (with bile salts reabsorption)

Two coenzymes of cobalamin are formed in the liver:
5-deoxy-aadenosyl-cobalamin
Methyl-cobalamin (THF donates a methyl group to cobalamin)

43
Q

What are the primary functions of cobalamin?

A

B12 is required as coenzyme to primarily two enzymes

- L-methyl malonyl-coA mutase
- Methionine synthase
  1. 5-Deoxy adenosyl cobalamin required by L-methyl malonyl-coA mutase to catalyse the conversion of L-methyl malonyl-CoA to succinyl-CoA. Succinyl CoA enters the CAC for energy production
    • If this reaction does not occur, L-methyl malonyl CoA is converted to methylmalonic acid (MMA). Excess MMA results in synthesis of abnormal myelin FA. These abnormal FA are incorporated as part of the weak myelin sheath in the nervous system. Abnormal myelination/demyelination can occur: severe CAN and PNS dysfunctions may develop
  2. Methyl-cobalamin is required as a coenzyme for methionine synthase function
    • Conversion of homocysteine (AA not found in diet) to methionine
    • Since methyl-cobalamin formation depends on folate, if both or either folate or B12 are low in supply, homocysteine builds up
    • Homocysteine can also reform methionine when receiving a methyl group from betaine or can form cysteine via trans-sulphuration, requiring vitamin B6
    • If protein intake is high, and vitamin B6, folic acid, and B12 are low, homocysteine builds up. High levels associated with CVD
44
Q

What are the requirements for B12?

A

RDI, no UL

Older adults may need 2-3x the RDI due to atrophic gastritis

45
Q

Describe the signs and symptoms of cobalamin deficiency

A

Megaloblastic/macrocytic RBC (like in folate deficiency) and anaemia

Overtime: paraesthesia, severe nerve degeneration (loss of myelin sheath)

Poor concentration/memory, dementia

46
Q

What are the causes of cobalamin deficiency?

A

Pernicious anaemia (=leading to death): death within 2-5 years due to the lack of mature RBC

Absence of R-protein (from stomach and saliva)

Poor binding of the IF-B12 complex (receptor polymorphism)

Presence of B12 consuming bacteria in the ilium

Anti-acid medications: reduced HCl production => reduced freeing of B12

Atrophic gastritis resulting from ageing => parietal cells loose function

Crohn’s and Coeliac disease

Vegan or other exclusion diets without supplementation or using fortified foods

Metformin (T2DM medication): interferes with B12 absorption

47
Q

What are some good food sources of B12?

A

Oysters, liver

48
Q

Describe the absorption, transport, storage and excretion of choline

A

Not technically a “vitamin” => can be synthesised by the liver

- Does not function as a coenzyme
- Present in large amounts in the body

Absorption: Small intestine via transport protein

Transport: From liver, circulates free to other tissues, uptake in cells by diffusion and via carrier proteins (blood brain barrier)

Storage: Small amount in the liver

Excretion: Mostly oxidised in the liver as betaine. Excess excreted via the urine

49
Q

What are the primary functions of choline?

A
  1. Is part of phospholipids , lipoproteins, cell membrane, sphingomyelin
  2. Precursor of acetylcholine: essential in brain and muscle function as neurotransmitter
  3. Homocysteine metabolism: methyl donor in the conversion of homocysteine to methionine as betaine
50
Q

Describe the requirements for choline

A

AI and UL

51
Q

Describe the signs and symptoms of choline deficiency

A

Fatty liver, kidney and liver damages = essential despite liver production possible

52
Q

What forms of vitamin C are there?

A

Dehydro-ascorbic acid = oxidised form (must be reduced)

Ascorbic acid = reduced form (can act as an electron donor)

53
Q

Describe the absorption, transport, storage and excretion of vitamin C

A

Absorption:

- Small intestine
- Ascorbic acid: active transport
- Dehydro-ascorbic acid: facilitated diffusion, then reduced to ascorbic acid
- Absorption declines at greater dosage (in single dosage)

Transport: As ascorbic acid in the blood

Storage:

- Pituitary gland, adrenal glands, WBC, eyes, brain
- Body pool of 300-400mg at any one time

Excretion:

- Excess filtered by kidneys and excreted via the urine, rapid excretion in urine above 100mg/day
- Conserved by kidneys when in short supply
54
Q

What are the functions of ascorbic acid?

A
  1. Electron donor to free radicals, non-specific reducing agent
  2. Cofactor to metalloenzymes: keeps the metal ions in metalloenzymes in the reduced form
  3. “Recycles” vitamin E and dehydro-ascorbic acid by reducing them
  4. Assists in non-haem iron absorption (by reduction to ferrous iron form)
  5. Collagen synthesis: proline and lysine in the protein strands are hydroxylated to form hydroxyproline and hydroxylysine by lysil and prolyl hydroxylases.
    • This allows for the triple helix of strong collagen to form
    • Ascorbic acid keeps the iron in prolyl and lysil hydroxylases in the reduced (ferrous Fe2+) form => formation to strong collagen
55
Q

What are the requirements for vitamin C?

A

RDI and UL

56
Q

Describe the signs and symptoms of vitamin C deficiency and toxicity

A

Deficiency = scurvy
Inadequate synthesis of strong collagen
Haemorrhages, bleeding gums, diarrhoea

Above UL = increased risk of kidney stones when there is a predisposition

57
Q

What are the most common causes of vitamin C dificiency?

A

Poor nutrition, poverty
Infants in developing countries
Smokers
Alcoholism

58
Q

What are some good food sources of vitamin C?

A

Guava, red pepper, kiwi, strawberries

Fruits and veggies

NUTR2101 (13 decks)

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