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Gastrointestinal Biology > GB 10. Digestion and Absorption of Lipids. The Handling of Iron in the Body > Flashcards

GB 10. Digestion and Absorption of Lipids. The Handling of Iron in the Body Flashcards

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1
Q

What is the structure of a triacylclycerol?

A
  • 1 glycerol molcules

- 3 fatty acid chains

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2
Q

What is a saturated fatty acid?

A

fatty acid with NO double bonds

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3
Q

What is monounsaturated fatty acids?

A

fatty acid with 1 double bond

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4
Q

What is polyunsaturated fatty acids?

A

fatty acid with 2 or more double bonds

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5
Q

What are the 3 principle sites of lipid digestion? What is involved in each site?

A

[1] MOUTH

  • mastication
  • emulsification
  • lingual lipase

[2] STOMACH
- gastric lipase

[3] SMALL INTESTINE

  • pancreatic enzymes
  • emulsification
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6
Q

What is emulsification of lipids in the mouth? What does it allow for?

A
  • breakdown of large droplets of lipid into tiny droplets
  • requred for efficient digestion of lipids
  • allows enzymes to gain access to lipid substrates
  • starts with chewing (mastication)
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7
Q

What enzymes are involved in the breakdown of lipids in the stomach? Describe the enzymes a bit

A

[1] Lingual Lipase
[2] Gastric Lipase

  • both are lipases
  • relatively acid stable
  • act on TAGs with short to medium FA chains (less than 12 carbons)
  • important in neonates (to digest milk fat) and patients lacking pancreatic lipase [!!!]
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8
Q

Emulsification first occurs in the mouth, but is then further continued in…

A

the intestine

- specifically, the duodenum

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9
Q

What happens during emulsification in the intestine?

A
  • it increases the surface area of lipid droplets so enzymes can work at lipid/aqueous interface
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10
Q

How is emulsification of lipids in the small intestine achieved by? [2]

A

[1] Bile Salts - detergent properties

[2] Peristalsis - mechanical mixing

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11
Q

What are the pancreatic enzymes involved in the digestion of lipids? Explain some processes.

A

[1] Pancreatic Lipase
- binds to surface of droplet in presence of Pancreatic Colipase

[2] Colipase-Lipase Complex (Pancreatic Lipase)

  • spreads over surface of droplet
  • leads to hydrolysis of triglycerides to monoacylglycerol and fatty acids

[3] Cholesterol Esterase

  • hydrolyzes cholesteryl esters to cholesterol + free fatty acids
  • activity increased by bile salts

[4] Phospholipase A2

  • digests phospholipid to lysophospholipid by removing 1 fatty acid
  • activated by trypsin
  • requires bile salts for optimum activity

[5] Lysophospholipase

  • removes remaining fatty acid at C1
  • leaving glycerylphosphoryl base: excreted, further degraded or absorbed
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12
Q

The products of fat digestion are formed into what?

A

Mixed Micelles

  • bile salts
  • free fatty acids
  • free cholesterol
  • 2-monoacylglycerol
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13
Q

What do mixed micelles contain?

A

Mixed Micelles

  • bile salts
  • free fatty acids
  • free cholesterol
  • 2-monoacylglycerol
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14
Q

Explain how lipids are absorbed by enterocytes. [2]

A

[1] Micelle has Hydrophilic Surface

  • can cross water layer brush border of enterocyte
  • transports hydrophobic lipids across border

[2] Short/Medium Chain FAs
- do NOT require mixed micelles for absorption

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15
Q

After they are absorbed, lipids can be excreted from enterocytes to aid in chylomicron formation. Explain this.

A
  • fatty acids and monglyceride are transported into the ER where they are used to make TRIGLYCERIDE
  • triglycerides are grouped with:
  • – cholesterol esters
  • – free cholesterol
  • – phospholipids
  • – vitamins
  • – apolipoprotein B48
  • they form into chylomicrons
  • they then go to Golgi Apparatus
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16
Q

After the formation of chylomicrons, what happens to them?

A
  • they are excreted from Golgi Apparatus into EXOCYTOTIC VESICLES
  • transported to basolateral aspect (membrane) of enterocyte
  • the vesicles fuse with plasma membrane and undergo exocytosis
  • chylomicrons enter extracellular space and enter lymph
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17
Q

What are the primary products of lipid digestion?

A

[1] Free Fatty Acids
[2] Free Cholesterol
[3] 2-Monoacylglycerol

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18
Q

What is the secretion of pancreatic enzymes controlled by?

A

it is hormonally controlled

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19
Q

The absorption of lipids and fat-soluble vitamins (vitamin A,D,K,E) are dependent on 3 factors which are:

A

[1] Bile Salts
[2] Normal Pancreatic Function
[3] Normal Intestinal Cells

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20
Q

What are the causes of some Malabsorption syndromes?

A

[1] Pancreatic Insufficiency
- chronic pancreatitis

[2] Inadequate Mucosal Surface
- as in coeliac disease (gluten sensitivity) due to flattening of villi

[3] Inflammatory States

  • Crohn’s Disease
  • may affect entire bowel

[4] Infection
- acute (salmonella) or chronic (tropical sprue) leading to intestinal hurry

[5] Surgery
- surgical resection or fistulae of small bowel

[6] Cystic Fibrosis
- pancreatic enzyme deficiency

[7] Disaccharidase Deficiency

  • e.g. congenital or acquired lactase deficiency
  • or congenital sucrase-isomaltase deficiency
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21
Q

What are the symptoms of malabsorption? What is it normally accompanied by?

A
  • weight loss + weakness
  • failure to thrive (babies)

frequently accompanied by….

  • steathorrhoea (visible fat in stools)
  • intestinal discomfort
  • diarrohea
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22
Q

How is malabsorption usually detected?

A
  • endoscopy/biopsy
  • serum enzymes in case of pancreatitis

note: it MUST be treated!

23
Q

Not everything can be digested and some main examples are…

A

[1] digestion of most nutrients is incomplete

[2] Keratins + Plant Polymers (such as Cellulose + Pectin) are not digested

[3] some veggies contain Indigestible Carbs

24
Q

How much iron does the body normally contain?

A
  • 2 to 4 grams of iron
25
Q

What is the reduced form of iron?

A

Fe2+

- ferrous

26
Q

What is the oxidized form of iron?

A

Fe3+

- ferric

27
Q

What is the ferrous form?

A

Fe2+

- reduced

28
Q

What is the ferric form?

A

Fe3+

- oxidized

29
Q

A lot of iron in the body goes towards…

A
  • haemoglobin
30
Q

What are the 3 main categories that iron is used towards in the body?

A

[1] Haemoglobin
[2] Myoglobin + Enzymes
[3] Storage Iron

31
Q

What is the most common micronurient deficiency?

A

Iron Deficiency

32
Q

When iron levels drop, what happens?

A

[1] storage iron is mobilized first

[2] haemoglobin synthesis is impaired

33
Q

What can iron deficiency result in?

A

results in microcytic hypochromic anaemia

34
Q

How do you treat iron deficiency?

A

iron supplements

35
Q

What is Haemosiderosis?

A
  • accumulation of ferritin and hemosiderin

- leads to free radical generation

36
Q

What is Haemochromatosis? What may it be caused by?

A
  • progressive hemosiderosis
  • results in organ damage
  • associated with a mutation in HFE gene (human hemochromatosis protein)
37
Q

How do you treat iron overload?

A

[1] Repeated Phlebotomy

[2] Iron Chelator: Desferrioxamine

38
Q

What are the 2 major forms of dietary iron?

A

[1] Haem Iron

[2] Non-Haem Iron

39
Q

What is haem iron derived from? How is it absorbed?

A
  • derived primarily from haemoglobin + myoglobin in animal protein sources (red meat)
  • it must be hydrolyzed from any protein it is attached to first
  • then absorbed readily but slowly

overall absorption from meat is about 20 to 25%

40
Q

Where does Non-Haem Iron come from?

A
  • bound to some other organic constituent of food (cereals, pasta, beans, dark green leafy veggies)
  • cooking tends to break these interactions and increase iron availability
41
Q

What are the 2 changes of oxidation state that iron undergoes during digestion and absorption? Describe the change of state, location and so on.

A

[1] Fe3+ reduced to Fe2+

  • stomach
  • favoured by low pH (HCl)
  • reducing agents (like ascorbic acid) assist the process
  • *reduction important as Fe2+ dissociates from ligans more easily than Fe3+

[2] Fe2+ oxidized to Fe3+

  • duodenum (bicarbonate rich and alkaline)
  • in alkaline environment, haem absorbed directly by mucosal cells
  • within mucosal cells, iron dissociates from it
  • free Fe2+ oxidized to Fe3+ and taken up by mucosal cells
42
Q

How is haem aborbed? What is the transporter involved?

A
  • haem absorbed entirely into the enterocyte
  • transporter: Haem Carrier Protein 1
  • Fe2+ is released from haem by haem oxidase
43
Q

Which transporter moves haem into the enterocyte?

A

Haem Carrier Protein 1

44
Q

How is Non-Haem Iron absorbed into the enterocyte?

A
  • Fe3+ is reduced by the reductase Duodenal Cytochrome B (DcytE) to Fe2+
  • Fe2+ transported into enterocyte via Divalent Metal Transporter 1 (DMT1) only!
45
Q

What are the 2 fates of iron after entering the enterocyte?

A

[1] stored as cystolic iron as Ferritin

[2] transported across the basolateral membrane via Ferroportin (FPN)

  • Fe2+ converted back to Fe3+ by Hephaestin
  • Fe3+ binds to Transferrin for transport around body
46
Q

What happens to iron after it enter the blood circulation?

A
  • Fe2+ converted back to Fe3+ by Hephaestin

- Fe3+ binds to Transferrin for transport around body

47
Q

Iron absorption is reduced by the presence of…[5]

A 
[1] Tannins
[2] Oxalate
[3] Phytate
[4] Inorganic Phosphates
[5] Phosphate containing Antacids
48
Q

What is iron deficiency anaemia a result of?

A

a result of poor iron absorption

49
Q

What is apotransferrin?

A

transferrin without a Fe3+

50
Q

Where does transferrin-bound iron go to?

A

[1] to iron stores

[2] to bone marrow

51
Q

How does iron enter a cell? Explain the process.

A

[1] enters by endocytosis through a Transferrin Receptor

[2] a CURL (compartment of uncoupling of receptor and ligand) is formed

[3] Fe3+ is released and stored in ferritin in the cytoplasm of cell

[4] apotransferrin is recycled to surface of cell

52
Q

What is a CURL?

A

Compartment of Uncoupling of Receptor and Ligand

53
Q

What state is iron mostly stored in? Where and how is it stored?

A
  • mainly sotred in ferric state (Fe3+)
  • stored as part of complex ferritin
  • protein forms a shell that contains about 3000 Fe3+ in form of ferric oxide hydroxide (FeOOH) crystals

Gastrointestinal Biology (15 decks)

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