9 Ions, Vitamins and Minerals Flashcards

1
Q
Q: mM
µM
nM
pM
fM
A
A: Millimolar 	(mM) 	10-3
Micromolar 	(µM) 	10-6
Nanomolar 	(nM) 	10-9 
Picomolar 	(pM) 	10-12 
Femtomolar 	(fM) 		10-15
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2
Q

Q: What is diffusion? How does speed vary? (2) How have multicellular organisms evolved? to?

A

A: The process whereby atoms or molecules intermingle because of their random thermal motion

Diffusion occurs rapidly over microscopic distances, but slowly over macroscopic distances.

Multicellular organisms evolve circulatory systems to bring individual cells within diffusion range

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3
Q

Q: What does the cell membrane act as in terms of diffusion? allowing? Which molecules can cross easily?

A

A: The cell membrane acts as a diffusion barrier, enabling cells to maintain cytoplasmic concentrations of substances different from their extracellular concentrations

Lipid soluble (non-polar) molecules can cross more easily than water soluble (polar) molecules

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4
Q

Q: What is osmosis?

A

A: water movement from hypotonic -> isotonic -> hypertonic ACROSS semipermeable membrane

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5
Q

Q: How does the epithelium of the gut form a continuous layer? What else does this structure do? What determines the molecules that can cross the epithelium to enter the bloodstream?

A

A: tight junctions form between enterocytes- different proteins that connect cells together

allows differentiation between apical and basolateral membrane as proteins can’t move freely between the regions

depends on ‘tightness’- not consistent throughout the gut -> have varying leakiness/selectivity on what can pass between cells

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6
Q

Q: What are the 2 ways molecules can cross the epithelium to enter the blood?

A

A: Paracellular Transport
through tight junctions and lateral intercellular spaces.

Transcellular Transport through the epithelial cells (absorbed at apical side of cell and exocytosed on other (basolateral))

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7
Q

Q: What are the 3 ways that solutes can cross cell membranes? What are the 2 types of protein involved? Speed comparison? Control comparison?

A

A: simple diffusion, facilitated transport or active transport. Two types of transport proteins involved.

1) Channel proteins form aqueous pores allowing specific solutes to pass across the membrane.
2) Carrier proteins bind to the solute and undergo a conformational change to transport it  across the membrane.

Channel proteins allow much faster transport than carrier proteins but channel proteins allow much less control - only allow things to move DOWN electrochemical gradient
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8
Q

Q: What are the 4 types of ion channel?

A

A: can be gated to some degree- can be open or closed

  1. voltage gated
  2. ligand-gated (extracellular ligand) eg H binding
  3. ligand-gated (intracellular ligand) - secondary intracellular signals eg cAMP or Ca2+
  4. mechanically gated eg pressure transducers and stretch receptors
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9
Q

Q: What are the 3 types of carrier mediated transport?

A

A: uniport- allows the movement of 1 molecule in 1 direction

coupled transport:

symport- allows the movement of 2 molecules in one direction

antiport=counter transport: allows movement of 2 molecules in opposite directions (often of molecules with same charge= prevent disturbance of electrochemical equilibrium)

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10
Q

Q: What are the 3 types of membrane transport in terms of energy? Describe.

A

A: Active transport requires energy:

  • Primary active transport is linked directly to cellular metabolism (uses ATP to power the transport).
  • Secondary active transport derives energy from the concentration gradient of another substance that is actively transported = currency is often Na+

Facilitated transport /facilitated diffusion:
-enhances the rate a substance can flow down its concentration gradient. This tends to equilibrate the substance across the membrane and does not require energy

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11
Q

Q: Give 2 examples of Primary active transporters.

A

A: Na+/K+ ATPase

H+/K+ ATPase (in stomach- H+ put into gastric fluid)

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12
Q

Give 3 examples of Secondary active transporters.

A

A: SGLT-1 co-transport (sodium/glucose)

HCO3-/Cl- counter transport (in pancreas)

Na+/H+ counter transport (in pancreas)

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13
Q

Q: Give 2 examples of Facilitated transport /facilitated diffusion transporters. we have already covered in the course.

A

A: GLUT-5, GLUT-2

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14
Q

Q: By which process are glucose and galactose absorbed by enterocyte? Via? When is this effective? why?

A

A: by secondary active transport (carrier protein and electrochemical gradient)

Carrier protein = SGLT-1 on apical membrane

SGLT1 can transport glucose uphill against its concentration gradient (so effective when glucose at levels in the lumen are below those in the enterocyte)
- energy is being inputted in form of Na+ coming down its electrochemical gradient

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15
Q

Q: By which process is fructose absorbed by enterocyte? Via? When is this effective? why?

A

A: Absorption of fructose is by facilitated diffusion

Carrier protein = GLUT-5 on apical membrane

Effective at relatively low concentrations of fructose in the lumen as tissue and plasma levels are low

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16
Q

Q: By which process does glucose exit an enterocyte? Via? How does glucose vary between plasma and tissue/enterocyte?

A

A: Exit of glucose at the basolateral membrane is by facilitated diffusion. Carrier protein = GLUT-2, a high-capacity, low-affinity facilitative transporter.

Glucose between plasma and tissue/enterocyte generally equilibrated.

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17
Q

Q: What percentage of H2O presented to the GI tract is absorbed? What powers this absorption? speed? Where in the GI tract is the greatest amount of water absorbed?

A

A: 99%

by the absorption of ion- Many ions slowly absorbed by passive diffusion

in the small intestine, esp the jejunum

18
Q

Q: What can describe calcium and iron absorption? means?

A

A: Calcium and iron are incompletely absorbed by specific mechanisms, and this absorption is regulated

19
Q

Q: Approximately, how many litres of water a day is absorbed by 2 named organs? Compare. How does this compare to how much we drink?

A

A: Approximately 8 litres of water a day absorbed in the small intestine.

Approximately 1.4 litres of water a day absorbed in the large intestine (works harder and content is more solid)

we don’t drink that much, the rest of the water absorbed is from secretions

20
Q

Q: Name 6 contributors to the water in our gut (predominantly reabsorbed). Include how many litres they put into gut?

A

A: ingest 2L

saliva 1.2L

gastric secretions 2L (stomach)

bile 0.7L

pancreas 1.2L

intestinal 2.4L

21
Q

Q: What drives the water absorption in the gut? DIAGRAM. How does it create this environment? (4) Include the absorption of 3 other ions.

What occurs next to the ions? What does this change? What happens to water? (3)

What occurs to the driving force?

A

A: Na+ primarily

4 mechanisms that put Na+ into enterocytes and increase intracellular concentration

  1. Counter-transport in exchange for H+ (proximal bowel)
  2. Co-transport with amino acids, monosaccharides (jejunum) (SGLT-1)
  3. Co-transport with Cl- (ileum) (opposite charges = equalises)
  4. Restricted movement through ion channels (colon) (on its own through aqueous pore/ ion channel)
  • Cl- co-transported with Na+ (ileum)
  • Cl-exchanged with HCO3- (colon) into enterocytes. Both secondary active transport.
  • K+ diffuses in via paracellular pathways (tight junctions) in small intestine, leaks out between cells in colon. Passive transport
  1. Cl- and HCO3- transported into the intercellular spaces due to electrical potential created by the Na+ transport.
  2. High conc of ions in the intercellular spaces causes the fluid there to be hypertonic
  3. Osmotic flow of water from the gut lumen via adjacent cells, tight junctions into the intercellular space.
  4. Water distends the intercellular channels and causes increased hydrostatic pressure.
  5. Ions and water move across the basement membrane of the epithelium and are carried away by the capillaries.

What happens to this intracellular sodium?
Active transport of Na+ into the lateral intercellular spaces by Na+K+ATPase transport in the lateral plasma membrane

22
Q

Q: What is standing osmotic gradient?

A

A: reabsorption of water against the osmotic gradient in the intestines

23
Q

Q: Where does the majority of Ca2+ absorption occur? How can Ca2+ in your diet affect gut absorption? What stimulates absorption? (2) Usually?

A

A: Duodenum and Ileum absorb Ca2+

Ca2+ deficient diet increases gut’s ability to absorb.

Vit D and parathyroid hormone stimulate absorption.

usually don’t need to stimulate lots as diet contains so much

secretions 0.6g. Absorb 0.7g so we only need 0.1g, BU T out diet is 1-6g/day,

24
Q

Q: What’s the concentrationof Ca2+ in intracellularly? why? extracellularly? (2)

A

A: Low intracellular [Ca2+] approx 100 nM (0.1µM)
(but can increase 10– to 100-fold during various cellular functions)
=> try and keep low as it’s an intracellular signaller

High extracellular fluid [Ca2+] approx 1-3mM.
(Plasma [Ca2+] approx 2.2-2.6mM)
(Luminal [Ca2+] varies inmM range)

25
Q

Q: Calcium movement. How is it carried across apical membrane? Why does it need making inert? How?

A

A: i) Intestinal calcium-binding protein (IMcal)- facilitated diffusion.

ii) Ion channel

it’s a intracellular signaller-> when you absorb high levels you don’t want to start up all the intra processes-> need a way of making inert => done by binding to calbindin in cytosol

26
Q

Q: How is Ca2+ moved across the basolateral membrane? (2) Compare affinity and capacity. Main difference? Why does it have 2 mechanisms?

A

A: 1. by plasma membrane Ca2+ ATPase (PMCA) against concentration gradient

  • PMCA has a high affinity for Ca2+ (but low capacity- not that fast)
  • Maintains the very low concentrations of calcium normally observed within a cell.
  1. by plasma membrane Na+/Ca2+ exchanger against concentration gradient
    - The Na+/Ca2+ exchanger has a low affinity for Ca2+ but a high capacity.
    - Requires larger concentrations of Ca2+ to be effective.

allows you to shift between Ca2+ dynamics effectively (work in conjunction with one another)

27
Q

Q: What is vitamin D essential for? Deficiency causes? (2) What form is taken up by cells? What does it do when enterocytes take it up? (3)

A

A: normal Ca2+ absorption

Deficiency causes rickets, osteoporosis.

1, 25-dihydroxy D3 taken up by enterocytes:

  • Enhances the transport of Ca2+ through the cytosol
  • Increases the levels of calbindin
  • Increases rate of extrusion across basolateral membrane by increasing the level of Ca2+ ATPase in the membrane.
28
Q

Q: How can iron act? (2) What processes in the body is iron critical for? (2) What are the implications for iron absorption? (2)

A

a: electron donor and an electron acceptor

Oxygen transport (red blood cells)

Oxidative phosphorylation
(mitochondrial transport chain)

  • Iron is toxic in excess, but the body has no mechanism for actively excreting iron.
  • Need to be able to absorb quickly as required, but also to limit that absorption.
29
Q

Q: How much iron does an adult ingest? absorbs? Iron in diet is present as? (2) eg (2,3). Which form is more readily absorbed?

A

A: Adult ingests approx 15-20mg/day
but absorbs only 0.5-1.5mg/day.

Iron present in the diet as:
a) inorganic iron (Fe3+ ferric, Fe2+ ferrous)
b) as part of heme (haem) group
(haemoglobin, myoglobin and cytochromes).

Heme smaller part of diet, but more readily absorbed (20% of presented, rather than 5%)

30
Q

Q: What does Fe3+ readily form? eg (3). What reduces it to Fe2+? Which form of iron can we absorb?

A

A: insoluble salts

  • hydroxide
  • phosphate
  • HCO3-

vitamin C

Fe2+, can’t absorb Fe3+

31
Q

Q: What is heme? Describe dietary haem. Absorption? via? Liberation of iron?

A

A: coordination complex “consisting of an iron ion coordinated to a porphyrin acting as a tetradentate ligand, and to one or two axial ligands.”

Dietary heme is highly bioavailable.

Heme is absorbed intact into the enterocyte.
Evidence that this occurs via heme carrier protein 1 (HCP-1), and via receptor-mediated endocystosis.

Fe2+ liberated by Heme oxygenase. (in ER)

32
Q

Q: Describe the process of iron uptake. (3) What happens when it arrives in the blood? (3)

A

A: 1. Duodenal cytochrome B (Dcytb) catalyzes the reduction of Fe3+ to Fe2+ in the process of iron absorption in the duodenum of mammals.

  1. Fe2+ transported via divalent metal transporter 1 (DMT-1), a H+-coupled co-transporter.
  2. Fe2+ binds to unknown factors, carried to basolateral membrane
  3. moves via ferroportin ion channel on basolateral membrane into blood.
  4. Hephaestin is a transmembrane copper-dependent ferroxidase (associated with ferroportin) that converts Fe2+ to Fe3+.
  5. Fe3+ binds to apotransferrin, travels in blood as transferrin.
33
Q

Q: What is the main hormonal control of iron absorption? result?

A

A: Hepcidin, the major iron regulating protein, suppresses ferroportin function to decreases iron absorption

34
Q

Q: Why should we prevent the absorption of excess iron? How? (3) Result? What happens in excess dietary iron absorption?

A

A: =(toxic).

Irreversible binding of iron to ferritin in the epithelial cells.

  1. binds to apoferritin in cytosol to form ferritin micelle = Ferritin is globular protein complex.
  2. Fe2+ is oxidised to Fe3+ which crystallises within protein shell.
  3. A single ferritin molecule can store up to 4,000 iron ions.

since in 3+ form can’t be absorbed-> when cells slough off -> lose Fe3+ back into luminal gut -> excreted in the faeces

produce more ferritin (Increase in iron concentration in the cytosol increases ferritin synthesis)

35
Q

Q: What are vitamins? (2) How are they predominantly absorbed? Others? (3) Examples (4,1,4)

A

A: Organic compounds that cannot be manufactured by the body but vital to metabolism.

Passive diffusion predominant mechanism

  • Fat soluble vitamins (A, D, E, K) transported to brush border in micelles (solubilised)
  • K taken up by active transport.
  • Specific transport mechanisms for vitamin C (ascorbic acid), folic acid, vitamin B1 (thiamine), vitamin B12
36
Q

Q: Where is Vitamin B12 stored? How much? What does impaired absorption of vit B12 do? name? Cause? (2) How is most B12 found in food? liberated where?

A

A: Liver contains a large store (2-5mg).

retards the maturation of red blood cells - pernicious anaemia.

  • lack in diet
  • genetic disorder

Most Vit B12 in food is bound to proteins

37
Q

Q: How is B12 liberated? where? Downside? How is it avoided?

A

A: In the stomach, low pH and the digestion of proteins by pepsin releases free vit B12.

But B12 is easily denatured by HCl.

-Binds to R protein (haptocorrin) released in saliva and from parietal cells

38
Q

Q: Describe the process from B12 ingestion to absorption. (5)

A

A: 1. Vit B12 in food bound to proteins= liberated

  1. binds to R protein (haptocorrin) in stomach
  2. complex moves further-> R proteins digested in duodenum -> then need something else to transport from here to area in gut it will be absorbed
  3. binds to Intrinsic Factor (IF) (Vit B12 binding glycoprotein) secreted by parietal cells -> Vit B12/IF is resistant to digestion.

No IF then no absorption of vit B12

  1. Vit B12/IF complex binds to cubilin receptor, taken up in distal ileum (mechanism unknown, but thought to involve receptor-mediated endocytosis).
39
Q

Q: Why doesn’t B12 bind to Intrinsic Factor (IF) ( Vit B12 binding glycoprotein) rather than R protein (haptocorrin) in stomach?

A

A: R protein has higher affinity for B12

40
Q

Q: What happens to B12 once in an enterocyte? (6) in what form?

A

A: 1. Once in cell, Vit B12/IF complex broken- possibly in mitchondria

  1. B12 binds to protein transcobalamin II (TCII)
  2. crosses basolateral membrane by unknown mechanism
  3. Travels to liver bound to TCII.
  4. TCII receptors on cells allow them to uptake complex.
  5. Proteolysis then breaks down TCII inside the cell.