12. Ions, vitamins and minerals Flashcards

1
Q

Describe the absorption of glucose & galactose

A
  • SGLT-1
  • Secondary active transport
  • Carrier protein & electrochemical gradient
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2
Q

Describe the absorption of fructose

A
  • GLUT-5
  • Facilitated diffusion
  • Effective at low concentrations in the lumen as tissue/plasma levels are low
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3
Q

Describe the exit of glucose into the blood

A
  • GLUT-2
  • Facilitated diffusion
  • High-capacity, low-affinity
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4
Q

Outline the absorption of water

A
  • 99% of H2O presented to the GIT is absorbed
  • Powered by absorption of ions
  • Most absorbed in the jejunum
  • 8L a day in small intestine
  • 1.4L a day in large intestine
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5
Q

Where does the absorbed water come from?

A
  • Ingest (2L)
  • Saliva (1.2L)
  • Gastric secretions (2L)
  • Bile (0.7L)
  • Pancreas (1.2L)
  • Intestinal (2.4L)
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6
Q

How is a gradient created for the osmosis of water?

A

• Na+ transported from lumen into enterocyte
- counter-transport, H+ exchange (proximal bowel)
- co-transport with amino acids, monosaccharides (jejunum)
- co-transport with Cl- (ileum)
- restricted movement through ion channels (colon)
• Active transport of Na+ back out
- into lateral intercellular spaces
- sodium/potassium ATPase
- causes transport of Cl- and HCO3- out as well
- creates hypertonic intercellular fluid
- water moves out and distends these channels
- ions and water carried away by capillaries

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7
Q

How is Cl- absorbed into the GIT?

A
  • Ileum - co-transported with Na+
  • Colon - exchanged with HCO3-

(both secondary active transport)

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8
Q

How is K+ absorbed into the GIT?

A
  • K+ diffuses in via paracellular pathways (small intestine)
  • Leaks out between cells (colon)
  • Passive transport
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9
Q

How is calcium absorbed into the small intestine and blood?

A

• Duodenum and ileum

1) Intestinal calcium-binding protein - facilitated diffusion
2) Ion channel

  • Binds to calbindin in cytosol
  • This prevents its action as an intracellular signal

• Pumped across basolateral membrane by:

1) Ca2+ ATPase (PMCA) against concentration gradient
- High affinity, low capacity
- Maintains the low intracellular calcium concentrations
2) Na+/Ca2+ exchanger
- Low affinity, high capacity
- Requires larger concentrations of Ca2+ to be effective

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10
Q

How does intracellular and extracellular calcium compare

A
  • Low intracellular Ca2+ (100nM)

* High extracellular Ca2+ (1-3mM)

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11
Q

What affects the absorption of calcium into the small intestine and what is the standard absorption?

A
  • Ca2+ deficient diet increases gut’s ability to absorb
  • Vitamin D and parathyroid hormones stimulate absorption
  • Diet 1-6g/day
  • Secretions - 0.6g, absorb - 0.7g
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12
Q

What is the role of Vitamin D in calcium absorption?

A
  • 1,25-dihydroxy D3 is taken up by enterocytes
  • Enhances the transport of Ca2+ through the cytosol
  • Increases the levels of calbindin
  • Increases the rate of extrusion across basolateral membrane - increases Ca2+ ATPase
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13
Q

What is iron used for in the body?

A
  • Electron donor/acceptor
  • Oxygen transport
  • Oxidative phosphorylation
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14
Q

What are the implications for iron absorption?

A

• Needs to be absorbed quickly as required
• Absorption also needs to be limited
- toxic in excess
- no active excretion mechanisms

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15
Q

How is iron present in the diet, and how much is ingested and absorbed?

A
  • Inorganic iron (Fe2+ - ferrous, Fe3+ - ferric)
  • 20% of presented iron from heme is absorbed
  • Ingested - 15-20mg/day
  • Absorbed - 0.5-1.5mg/day
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16
Q

How is Fe3+ absorbed?

A

• Cannot be absorbed
• Forms an insoluble salt with hydroxide, phosphate and bicarbonate
• Duodenal cytochrome B (on brush border) reduces Fe3+ to Fe2+
• Vitamin C also reduces Fe3+
• DMT1 (divalent metal transporter 1) on apical membrane of enterocytes
- Fe2+ transported in
- H+-coupled co-transporter

17
Q

How does heme provide iron?

A
  • Highly bioavailable
  • Absorbed intact into the enterocyte (heme carrier protein 1 - HCP-1)
  • Fe2+ liberated by Heme oxygenase
18
Q

What happens to iron once it is in the enterocyte

A

Movement into blood
• Fe2+ binds to unknown factors, carrier to basolateral membrane
• Hephaestin (transmembrane copper-dependent ferroxidase) coverts Fe2+ to Fe3+
• Fe3+ moves into blood (ferroportin ion channel)
(• Hepcidin suppresses ferroportin function)

Storage
• Fe2+ can bind to apoferritin => ferritin (becomes ferrous Fe3+, which crystallises within protein shell)
• Excess dietary iron absorption => more ferritin
• Irreversible process
• Lost in intestinal lumen and excreted in faeces

19
Q

What are vitamins and how are they absorbed?

A
  • Organic compounds that cannot be manufacture by the body but vital to metabolism
  • Fat soluble vitamins (ADEK) transported to brush border in micelles
  • Passive diffusion (predominantly)
  • K taken up by active transport
  • Specific transport mechanisms for vitamin C, folic acid, vitamin B1 (thiamine) and vitamin B12
20
Q

Where is vitamin B12 found in the body?

A
  • Important in every cell
  • Liver contains a large store (2-5mg)
  • Most vitamin B12 in food is bound to proteins
21
Q

Where does free vitamin B12 in the stomach come from?

A
  • Low pH and digestion of proteins by pepsin

* Releases free vitamin B12

22
Q

How does vitamin B12 avoid denaturation in the stomach?

A
  • Binds to R protein (haptocorrin)
  • R protein is released in saliva and parietal cells
  • R proteins are digested in the duodenum
23
Q

What is intrinsic factor?

A
  • Glycoprotein produced by parietal cells
  • Vitamin B12 binds to it, resisting digestion
  • The complex binds to the cubulin receptor in the distal ileum
  • Taken up into enterocytes
24
Q

What is pernicious anaemia?

A
  • Immune system attacks cells in stomach producing intrinsic factor
  • Vitamin B12 cannot be absorbed if it’s not in a VitB12/IF complex
25
Q

What happens to the VitB12/IF complex once it enters the cell?

A
  • Complex is broken (possibly in mitochondria)
  • Vitamin B12 binds to transcobalamin II (TCII)
  • Crosses basolateral membrane by unknown mechanism
  • TCII-VitB12 complex travels to liver
  • TCII receptors allows liver to uptake the complex
  • Proteolysis breaks down TCII in the cells