Digestion And Absorption Part 1 DLA

Question 1

Summarize digestion in the mouth

Answer 1

Mainly Carbohydrate digestion
by salivary a-amylase
Salivary a-amylase cleaves a(1 4) glycosidic bonds of starch and
glycogen and it forms branched oligosaccharides.

Lingual lipase for lipid digestion is released in the oral cavity but is mainly swallowed.

Question 2

Summarize digestion in the stomach

Answer 2

• The thought of food, sight, smell, taste, chewing and a full stomach increases the release of gastrin from the gastric glands.
• Gastrin leads to the release of hydrochloric acid from parietal cells. The chief cells release pepsinogen and gastric lipase

Question 3

Why does HCl being a string acid medically relevant?

Answer 3

1. HCL denatures food for quicker digestion and destroys bacteria
   and fungi present in food.
2. HCL alters the conformation of pepsinogen in order for it to cleave itself: producing the active protease pepsin by autocatalytic activation.
3. Pepsin has a pH 2 optimum and cleaves peptide bonds within the protein (endopeptidase)

Question 4

What is the impact of low levels of gastric HCl?

Answer 4

1. Reduce the autocatalytic activation of pepsinogen to pepsin which
   leads to less effective digestion of proteins.
2. Are often found in the elderly due to the decline of HCl production
   with age.
3. Can result from excessive ingestion of antacids in individuals who use these drugs to treat acid reflux.

Question 5

What are the enzyme activities in the stomach?

Answer 5

1. Stop of carbohydrate digestion due to denatured salivary a- amylase at low pH. The enzyme is digested by pepsin.
2. Protein digestion starts performed by pepsin.
3. Lipid digestion of TAGs with medium-chain fatty acids starts performed by lingual and gastric lipases which degrade TAGs found in milk. The acidic pH allows digestion without the need for bile salts. Milk digestion generates free medium-chain fatty acids which are released into the portal vein and reach directly the liver for energy metabolism.

Question 6

Describe the release of secretin and cholecystokinin (CKK) from the endocrine cells of the duodenum

Answer 6

1. The acidic chyme reaches the duodenum resulting in release of secretin which leads to pancreatic bicarbonate secretion.
   The pH is changed to a neutral pH which is needed for pancreatic enzymes.
2. Fatty acids and amino acids generated by digestion in the stomach result in the release of CCK

Question 7

What are the actions of cholecystokinin?

Answer 7

Activation of:
1. the release of bile from the gallbladder. Bile is needed for lipid
digestion and absorption. Bile is also alkaline and leads to a neutral pH.

2. the enzyme enteropeptidase in the duodenum which cleaves
   trypsinogen to trypsin.
3. the secretion of pancreatic enzymes, zymogens and other proteins.

Inhibition of:
-the gastric motility which allows a pH change of the acidic chyme in
the duodenum using pancreatic bicarbonate and alkaline bile

Question 8

What is the function of bile salts on lipid difestion?

Answer 8

Lipid digestion and absorption
in the small intestine needs bile with bile salts

1. Bile salts emulsify the dietary TAGs for digestion by pancreatic lipase
2. Absorption of MAGs, cholesterol and fatty acids needs mixed micelles formed with bile salts.
3. Blockage of bile entering the duodenum by gallstones leads to dietary fat maldigestion and malabsorption

Question 9

What are bile salts?

Answer 9

Bile acids are amphipathic molecules with a hydrophilic and hydrophobic side..

E.g. cholic acid

Question 10

What is the regulated enzyme in bile acid synthesis?

Answer 10

Only the liver can synthesize bile acids from free cholesterol.
The regulated enzyme is cholesterol 7a-hydroxylase, a cytochrome P450 enzyme.

Question 11

Describe the bile acid chemical characteristics

Answer 11

• Bile acids have a pKa of 6 which indicates that 50% of molecules are uncharged (acid) and 50% are charged (base) at pH 6.
• A negative charge is wanted as it does not only improve lipid emulsification but it is needed for the hepatic ABC transporters for the release into the bile.

• Hepatic conjugation of bile acids with glycine or taurine changes
the pKa and leads to negatively charged molecules which are named “bile salts”

Question 12

How does the liver conjugate bile acids?

Answer 12

Liver conjugates bile acids with glycine or taurine and releases only the formed bile salts into bile

Question 13

How are secondary bile acids formed?

Answer 13

How are secondary bile acids formed
and what is the difference between a primary bile acid and a secondary bile acid?

• Bile salts are released by the liver, stored in the gallbladder and after CCK action, they emulsify dietary lipids in the duodenum, jejunum and ileum.
• In the terminal ileum bile salts are deconjugated by colonic bacteria to bile acids and to glycine and taurine.

• The bile acids synthesized in hepatocytes using free cholesterol are
named primary bile acids. Intestinal bacteria can now modify the
structure of these primary bile acids to generate secondary bile acids

Question 14

What are the names of primary & secomdary bile acids?

Answer 14

A mixture of primary and secondary bile acids/salts (95%) is reabsorbed mainly in the terminal ileum and reaches the liver via the hepatic portal vein.

This is known as the enterohepatic circulation of bile salts.

The liver conjugates both, primary and secondary bile acids and releases
again primary and secondary bile salts into the bile

Question 15

Only the oiver is involved with

Answer 15

1. Synthesis of primary bile acids using free cholesterol.
2. Conjugation of primary and secondary bile acids with glycine or taurine to form bile salts.
3. Release of bile salts and free cholesterol into bile for transport into duodenum. After that bile is needed for dietary lipid digestion and absorption.
4. Release of cholesterol into feces (directly by free
   cholesterol and indirectly by 5% of bile acids).