Physiology of Lipid Digestion

Question 1

What 3 areas does emulsion occur in?

Answer 1

Mouth (chewing), stomach (gastric churning and squirting through narrow pylorus), small intestine (segmentation and peristalsis).

Question 2

What are the 3 types of emulsion droplets and describe them?

Answer 2

1. multilamellar vesicle (two double layers). 2. Unilamellar vesicle (one double layer). 3. Mixed micelle (one single layer).

Question 3

How are emulsion droplets stabilised?

Answer 3

By addition of a coat of amphipathic molecules that form a surface layer on the droplets.

Question 4

What make up the amphipathic coat?

Answer 4

Fatty acids, monoacylglycerols, biliary phospholipids, cholesterol, bile salts (when droplets have progressively been reduced to unilammelar and mixed micelles).

Question 5

When is gastric lipase released and where from?

Answer 5

In response to gastrin, released from chief cells.

Question 6

Describe gastric lipase.

Answer 6

Has a pH optimum of 4 and is resistant to pepsin. Is inactive in the duodenum due to digestion by pancreatic protease and unfavourable pH, preferentially hydrolyses TAGs at the 3 position.

Question 7

What type of fatty acids are absorbed by the stomach?

Answer 7

Short and medium chain fatty acids.

Question 8

What do triglycerides get broken down into when digested by gastric lipase?

Answer 8

Diacylglycerol and a free fatty acid.

Question 9

What does the full activity of pancreatic lipase require?

Answer 9

Colipase co-factor, alkaline pH, calcium, bile salts and fatty acids.

Question 10

What position does pancreatic lipase usually hydrolyse triglycerides at?

Answer 10

The 1 and 3 positions.

Question 11

What other lipases are there?

Answer 11

Carboxyl ester hydrolase, phospholipase A2, lingual lipase.

Question 12

What pushes the vesicles apart when bile salts bind?

Answer 12

The negative charges on the surface of the vesicles.

Question 13

Describe the function of colipase.

Answer 13

Binds to the bile salts and lipase, allowing lipase to access tri and di-acylglycerols (as bile salts block access of lipase to TAGs).

Question 14

How do fatty acids enter the enterocytes from mixed micelles?

Answer 14

Passive diffusion and/or membrane fatty-acid translocases, fatty-acid binding protein and fatty-acid transport proteins.

Question 15

What happens to short or medium chain fatty acids in the enterocytes?

Answer 15

They exit through the basolateral membrane and enter the villus capillaries.

Question 16

What happens to long chain (>12 carbons) fatty acids and monoglycerides in the enterocytes?

Answer 16

They are resynthesised into triglycerides in the ER and are subsequently incorporated into chylomicrons.

Question 17

What protein allows the absorption of cholesterol?

Answer 17

Niemann-Pick-C1-like 1 protein (NPC1L1).

Question 18

What are the places where NPC1L1 is located?

Answer 18

Clatherin coated pits.

Question 19

What drug prevents cholesterol absorption and how?

Answer 19

Ezetimibe - binds to NPC1L1.

Question 20

Where does passive (paracellular) and active (transcellular) absorption of calcium occur?

Answer 20

Passive is whole length of duodenum. Active is mainly duodenum and upper jejunum.

Question 21

When calcium concentration in chyme is less than 5mM, what type of absorption predominates?

Answer 21

Active.

Question 22

What is active calcium absorption regulated by?

Answer 22

1,25-dihydroxyvitamin D3 (calcitriol), parathyroid hormone (increases 1,25-dihydroxyvitamin D3 synthesis).

Question 23

How does increased 1,25-dihydroxyvitamin D3 (calcitriol) lead to increased calcium transport?

Answer 23

It causes more expression of calcium channels on the apical membrane and Ca2+ATPase on the basolateral membrane.

Question 24

What does Fe2+ bind to in the stomach?

Answer 24

Gastroferrin.

Question 25

What reduces Fe3+ to Fe2+?

Answer 25

HCl, vitamin C, brush border cytochrome B ferric reductase.

Question 26

What transports iron into the enterocyte?

Answer 26

Divalent metal transporter 1 (DMT1) - coupled to H+ transport.

Question 27

What causes increased and decreased expression of DMT1?

Answer 27

Expression increased by blood loss, reduced by human haemochromatotis protein (HFE).

Question 28

What converts haem into Fe3+?

Answer 28

Haem oxidase.

Question 29

Where is ferroportin 1 located and what hormone negatively regulates it and when?

Answer 29

The basolateral membrane. Hepcidin is released from the liver when body iron levels are high.

Question 30

What causes vitamin B12 to be released from proteins when it is ingested?

Answer 30

Stomach acid.

Question 31

What binds to B12 in the stomach?

Answer 31

Haptocorin (secreted to saliva).

Question 32

What cells in the stomach release intrinsic factor?

Answer 32

Parietal cells.

Question 33

What digest haptocorin and where?

Answer 33

Pancreatic proteases in the small intestine.

Question 34

Where does B12 bind to intrinsic factor?

Answer 34

In the small intestine.

Question 35

Where and how is B12-intrinsic factor complex absorbed?

Answer 35

In terminal ileum by endocytosis.

Question 36

Why are vegans susceptible to B12 deficiency?

Answer 36

B12 is not present in vegetables.

Question 37

Describe the absorption of fat soluble vitamins?

Answer 37

Incorporated into mixed micelles -> usually passively transported into enterocytes -> incorporated into chylomicrons or VLDLs.

Question 38

What are the water soluble vitamins?

Answer 38

B complex vitamins (not B12), C and H.

Question 39

What are transport processes for water soluble vitamins similar to?

Answer 39

Those of monosaccharides, amino acids and small peptides. May be either Na+-dependent or independent.