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Health And Society > Week 6 > Flashcards

Week 6 Flashcards

1
Q

What are vitamins?

A

Essential micronutrients
• must be provided by dietary source
• compounds not synthesized by the host in amounts adequate to meet normal physiological needs

Organic compounds
• Distinct from other essential micronutrient minerals
• Distinct from other organic compounds in the diet, i.e. macronutrients (fats, carbohydrates, and proteins)
Natural components of foods, present in minute amounts
• Low intakes can cause deficiency diseases

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2
Q

Water-soluble vitamins

A
  • not readily stored - easily excreted
  • consistent daily intake is important
  • many synthesised by bacteria
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3
Q

Lipid-soluble vitamins

A
  • can accumulate in body
  • more likely to lead to hyperviterminosis
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4
Q

Functions of vitamin A

A
  • vision
    † Retinal binds to opsin to form rhodopsin in rods, iodopsin in cones
    † Essential for signalling
  • control of gene expression via transcription factors
    † Binding of retinoic acid activates receptors (RAR/RXR)
    † RAR/RXR bind DNA
    † Activate/repress gene expression
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5
Q

Vitamin A deficiencies

A

• Vision
† Nightblindness,
† Xerophthalmia (conjunctival ulcers)
• Teratogenic
† Excess is also teratogenic
† Crucial role of the Hox genes in embryogenesis
• Impaired immunity
• Anaemia
• Ostopenia
• Inappropriate bone depositio

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6
Q

Vitamin A toxicity

A

Causes
• Rarely from diet – sometimes consumption of animal livers
• Medication - 13-cis-Retinoic Acid (brand name ”Accutane”) can be used therapeutically to treat acne

Teratogenic
• Vitamin A effects expression of genes involved in embryogenesis

Idiopathic increased intracranial pressure
• Headache
• Vomiting
• Impairedconsciousness

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7
Q

Role of Vitamin D in Ca2+ homeostasis

A

• Vitamin D is involved in Ca2+ homeostasis
† Mediated by parathyroid hormone (PTH) – senses low Ca2+

• PTH promotes formation of active Vitamin D
† Negative feedback loop – High calcitriolàinactive PTH
† Homeostatic regulation

• Mechanisms:
†Renal reabsorption
† Intestinal absorption
† Mobilisation from bone (osteoclasts)

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8
Q

Vitamin D deficiency

A

Causes
• Provitamin D malabsorption
• Lack of UV

Osteomalacia (rickets)
• Low Ca2+
• Soft, pliable bones
• Impaired ossification

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9
Q

Vitamins K

A

K1 (phylloquinones)
K2 (menaquinones)

Found in plants
• e- acceptor in photosynthesis Converted from K1 by bacteria
• Found in fermented foods

Breaks naming convention
• named for German term meaning “coagulation vitamin”
(Koagulationsvitamin)

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10
Q

Function of Vitamin K: Gla proteins

A

Needed to activate Gla proteins
• Vit K is oxidised to quinone form
• Provides reducing power – acts as a cofactor for a carboxylase enzyme
• Adds a second carboxyl group to glutamic acid of certain proteins
• Glu residues → Gla residues

Effect
• Gla proteins can bind Ca2+
• Many proteins need to be carboxylated on glutamic acid residues to be active

To recycle oxidized Vitamin K it is reduced by 2 additional enzymes

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11
Q

Examples of Gla proteins

A

Blood coagulation
• Procoagulant: prothrombin (factor II), factors VII, IX, X
• Anticoagulant: proteins C, S, Z

Bone metabolism
• Osteoblast activity: Osteocalcin (Bone Gla Protein)
• Bone mineralisation: Matrix Gla protein (MGP)

Metabolism of blood vessels
• Arterial calcification: MGP

Tissue remodeling, cell fate changes
• Wound healing: Periostin

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12
Q

Vitamin K deficiency

A

Causes
• Abundant in diet, rare
• Lipid malabsorption
• Anticoagulant therapy
• Antibiotic therapy

Blood clotting disorders
• Important role of Gla proteins in coagulation factors and anticoagulant proteins
• Dangerous in newborns – injection given after birth

Osteoporosis
• Decreased activity of osteoblasts

Warfarin is a Vitamin K antagonist
• Over dose can be treated with Vit K

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13
Q

Vitamin E (tocopherol)

A

A family of tocopherols
(α-, β-, Ɣ-, δ-)

α-tocopherol
• highest biological activity
• most common

Dietary source
• Vegetable oils

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14
Q

Lipid Peroxidation

A

Caused by free radicals
• Fenton reaction (Fe2+) produces hydroxyl radical (OH-)
• Byproduct of metabolism
• Oxidative burst of immune cells

Lipid peroxidation is a chain reaction
• Oxidation of one lipid forms a free radical, oxidises further lipids

Targets
• PUFAs in biological membranes are susceptible

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15
Q

Vitamin E function

A

Enzyme cofactor
• α-tocopherol quinone acts as a cofactor of mitochondrial unsaturated FA synthesis

Antioxidant
• Stops free radical chain reactions
• Sacrificially oxidised to tocopheroxyl
• Can be recycled (reduced) back to tocopherol

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16
Q

Vitamin E deficiency and toxicity

A

Causes of deficiency
• Rarely from diet
• α-TTP mutations
• Fat malabsorption
• Peripheral neuropathy (Neurons: High levels of PUFA, Iron)
• Anemia, RBClifespan (RBC: High levels of PUFA)

Supra-physiological doses
• Stimulate immune system (e.g. Antibody production, mechanism is unclear)
• Cardiovascular health (Prevents oxidation of LDLs → involved in atherosclerosis)

Toxicity
• Rare, can tolerate large doses
• Antagonise functions of other fat - soluble vitamins (e.g. bleeding (VitK)

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17
Q

Vitamin C (Ascorbic acid)

A

• Synthesized by plants and other animals, but not humans
• Easily oxidized - not stable in stored or cooked foods
• Name comes from its “anti- scurvy” properties: “a-scorbic” vitamin

18
Q

Vitamin C functions

A

Cellular respiration
• Electron transport reactions

Antioxidant
• Redox recycling of ɑ-tocopherol, glutathione

Bioavailability of iron
• Ferrous form is more easily absorbed
• Ascorbate can reduce Fe3+ (ferric) → Fe2+ (ferrous)
• Increases transferrin - mediated iron uptake
• Increases ferritin translation, decreases ferritin degradation
• Increased storage of iron

Collagen synthesis
• Involved in hydroxylation of procollagen → stability of the protein

Immune system
• B and T-lymphocyte differentiation
• Phagocyte & leukocyte activity

19
Q

Vitamin C deficiency

A

Subclinical
• e.g.accumulation of lipid peroxidation products in retinal tissues

Scurvy
• Effect on collagen formation
† Mesenchymal tissues display signs
• Liver spots
• Spongy gums
• Bleeding from mucous membranes
• Lethargy
• Rheumatic pains
• Edema (swelling)
• Hemorrhage

Advanced Scurvy
• Open wounds
• Loss of teeth

20
Q

Vitamin B deficiencies

A

Causes relating to low intake
• Processed foods (white rice, white flour…)
† Mandatory fortification of grains with thiamin (B1) and folic acid
• Severe malnutrition

Causes relating to malabsorption
• Heavy alcohol use
† (especially thiamine B1, B3, folic acid B9, B6)
• Diseases which damage the intestines
† Inflammatory Bowel Disease (Crohn’s disease), Celiac Disease

Some genetic disorders affecting enzymes which have vitamins as a cofactor can mimic deficiency

21
Q

Vitamin B1 (thiamine or thiamin)

A

† Active coenzyme is thymine pyrophosphate (TPP)
† TPP is a cofactor for decarboxylation reactions in the action of many enzymes, including:
• pyruvate dehydrogenase
• α-ketoglutarate dehydrogenase
• transketolase (pentose phosphate pathway)

22
Q

Vitamin B1 deficiency

A

Mild
•GI complaints
• weakness

Moderate
• peripheral neuropathy
• mental abnormalities
• ataxia

Full-blown deficiency: “Beriberi”
• muscle wasting
• congestive heart failure
• delirium
• memory loss

• Now uncommon except in displaced (refugee) populations.
• Diet of polished (white) rice is a cause. Supplementing or rice bran ensures adequate intake.
† In Australia, bread must be fortified.
• Alcoholism can impair uptake and utilisation of B1 (Wernicke-Korsakoff syndrome)
• Acute complication of bariatric surgery (reduction of stomach size)

23
Q

Vitamin B2 (riboflavin)

A

Active coenzymes are
• flavin mononucleotide (FMN)
• flavin adenine dinucleotide (FAD)

FMN and FAD act as prosthetic groups in many redox enzymes in
• Carbohydrate metabolism (TCA cycle)
• b-oxidation of fatty acids
• The electron transport chain

24
Q

Vitamin B2 deficiency

A

• More common in displaced populations, poverty
• Can occur with malabsorptive syndromes (e.g. Celiac disease); anorexia nervosa
• Rare: inborn error of metabolism e.g. non-functional riboflavin transporter; riboflavin-dependent enzymes Vitamins are lost in processing many grains.
• Grain fortification: restores these nutrients.

• Mild, nonspecific symptoms
• Rarely occurs without other deficiency
• Inflammation of the lining of mouth and tongue
• Dry and scaling skin, keratitis, dermatitis
• Iron-deficiency anaemia
• Mental depression, forgetfulness

25
Q

Vitamin B3 (niacin)

A

2 forms (vitamers):
• nicotinic acid
• nicotinamide

Active coenzymes are :
• NAD+ (nicotinamide adenine dinucleotide)
• NADP+ (nicotinamide adenine dinucleotide phosphate)

26
Q

Biosynthesis of vitamin B3

A

† Liver can synthesise niacin from tryptophan
• Tryptophan is an essential AA
• 60 mg of tryptophanà1 mg of niacin
• Requires vitamin B6
† Gut bacteria may also convert TrpàNiacin
† Both processes are inefficient and very slow
† Effectively, Vitamin B3 (niacin) must be supplied in diet

27
Q

Vitamin B3 functions

A

NAD+ and NADP+ are cofactors in:
• Carbohydrate metabolism (glycolysis, TCAcycle)
• Pentose phosphate pathway
• β-oxidation of fatty acids
• Amino acid synthesis
• Nucleotide synthesis

28
Q

Vitamin B3 deficiency Pellagra (raw skin)

A

“the four D’s”:
• diarrhoea
• dermatitis
• dementia
• death

Milder deficiency
• Fatigue
• Irritability
• Poorappetite
• Headache

• Very rare. Maybe present in alcoholics, strict vegetarians, and populations with poor nutrition
• Some drugs inhibit conversion of tryptophan into niacin –including azathioprine (immunosuppressant), chloramphenicol (antibiotic), phenobarbital (anti-seizure medication)

29
Q

Vitamin B5 (Pantothenic Acid)

A

• Active coenzyme is acetyl CoA

CoA is a cofactor for
• TCA cycle
• Metabolism of fatty acids
• Formation of sterols (cholesterol and 7-dehydrocholesterol)

30
Q

Vitamin B5 deficiency

A

• “Burning feet” - distal paresthesias
• Gastrointestinal distress

Extremely rare
• Present in almost all foods
• Severe malnutrition
• Symptoms are somewhat non-specific

• Defects in pathway for CoA synthesis can occur
• Processing can cause losses (20-80%)
• Many processed foods are fortified (not mandatory in Australia for B5)

31
Q

Vitamin B6 (pyridoxine)

A

3 vitamers
• Pyridoxine, pyridoxal, pyridoxamine
• Active coenzyme is pyridoxalphosphate (PLP)

32
Q

Vitamin B6 functions

A

• Amino acid synthesis, glycogenolysis
• Cofactor for glycogen phosphorylase
• >100 enzymes for protein metabolism

Essential for :
• RBC metabolism, haemoglobin formation
• Nervous and immune system function

33
Q

Vitamin B6 deficiency

A

Neurological
• Depression
• Confusion
• Seizures

Skin
• Dermatitis
• Stomatitis
• Glossitis
Present in most foods, so it is rare
Occurs due to:
• Malabsorption
• Highlevelsofalcoholuse
• Pyridoxine–inactivatingdrugs
(eg. corticosteroids)
• Haemodialysis

34
Q

Vitamin B7 (biotin)

A

Coenzyme for several metabolic pathways
• Carbohydrates
• Fats
• Proteins

• Prosthetic group of several carboxylase enzymes
† Pyruvate carboxylase (gluconeogenesis)
† Acetyl CoA carboxylase (FAsynthesis)
• Is made by gut bacteria – unclear how much more is needed from diet

35
Q

Vitamin B7 deficiency

A

• Deficiency rarely caused by lack of intake
• Additionally, some synthesized by intestinal bacteria
• Symptoms are somewhat non- specific:
† Dermatitis around eyes, nose and mouth; alopecia
† Neurologic symptoms

Deficiency can be caused by other factors, including:
• Consumption of egg whites
† Protein (avidin) binds biotin very strongly
• Deficit in biotinidase enzyme – required to release protein- bound biotin, make biologically available

36
Q

Vitamin B9 (folate)

A

Active coenzyme is tetrahydrofolate (THF)

37
Q

Vitamin B9 functions

A

• THF is coenzyme of many transferases
• Role in nucleotide and nucleic acid synthesis

38
Q

Vitamin B9 deficiency

A

• Rare
• Is absorbed passively, and mediated by carrier

Symptoms:
• Anaemia (macrocytic)
• Peripheral neuropathy
• Increased circulating homocysteine (CVD risk)

Special case: pregnant people
• Deficiency: neural tube defects (Spina bifida) • Grains now supplemented
• Public health success story

39
Q

Vitamin B12 (cobalamin)

A

Metabolically active cofactors:
• Methylcobalamin (R: -CH3)
• Adenosylcobalamin (R: -Ado)

Cofactor for
• Energy synthesis
† FA oxidation
• DNA synthesis
• Methionine synthase

Essential for:
• RBC maturation
• Cell growth
• Formation of myelin
• DNA synthesis

40
Q

Vitamin B12 deficiency

A

30-40% of adults are deficient – develops slowly as body stores some B12
• Anaemia (reduced number RBC)
• Fatigue
• Decreased taste (loss of papillae / hyperpigmentation of the tongue)
• Reflex changes (reduced myelin synthesis, due to reduced methionine synthesis)
• Slowed mentation
• Can result in permanent nerve damage

Poor absorption
• Intestinal parasites, pernicious anemia, removal of stomach, genetic disorders

Improper management of vegetarian diet
• Not present in plant foods
• Present in yeast

Genetic disorders
• Receptor-mediated uptake – requires intrinsic factor

Health And Society (7 decks)

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