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Digestion And Metabolism > Digestion And Absorption > Flashcards

Digestion And Absorption Flashcards

1
Q

When does digestion start?

A

Digestion starts with the mouth and continues on in the stomach and small intestine.

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2
Q

What is absorption ?

A

Absorption of all macronutrients takes place in the intestinal mucosal cel

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3
Q

Where are carbs digested?

A

Carbohydrates (CHO) are digested in the mouth and small intestine.

Carbohydrates provide mainly glucose, galactose and fructose for energy metabolism. Glucose can be stored as glycogen

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4
Q

Where are proteins digested?

A

Proteins are digested
in the stomach and small intestine

Dietary proteins provide essential amino acids for synthesis of proteins and neurotransmitters.

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5
Q

When are lipids digested?

A

Lipids are digested
in the stomach and small intestine.

Dietary lipids provide essential fatty acids for membranes and eicosanoids. Fatty acids are used for energy metabolism or are stored in fat cells

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6
Q

When are nucleic acids digested?

A

Nucleic acids are digested in the small intestine.

Nucleic acids
Ribose, deoxyribose and pyrimidine bases are taken up into the liver. Purine bases are degraded in intestinal cells to uric acid and released in urine

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7
Q

Summarize the big picture if orotein digestion and absorption

A
  1. Mouth: proteins are not degraded.
  2. Stomach: pepsin degrades proteins to polypeptides and amino acids.
  3. Small intestine: pancreatic proteases form oligopeptides and amino acids.
  4. Brush border cells: aminopeptidases form peptides and amino acids.
  5. Intestinal mucosal cells: release of amino acids into the portal vein for
    transport to the live
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8
Q

How is trypsinogen activated by enteropeptidase?

A

Trypsinogen is released by the pancreas and is activated to trypsin only after it reaches the lumen of the duodenum.

This local separation prevents pancreatic damage as trypsin is a powerful protease and activates all other pancreatic zymogens

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9
Q

Explain the proteolytic activation of pancreatic zymogend

A

Once trypsinogen is activated by enteropeptidase, trypsin activates the following zymogens for protein digestion:

  • trypsinogen to trypsin
  • chymotrypsinogen to chymotrypsin
  • proelastase to elastase
  • procarboxypeptidases to carboxypeptidases

Trypsin also activates for lipid digestion:

  • prophospholipase A2 to phospholipase A2 - procolipase to colipase (protein
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10
Q

How pancreatic proteases cleave proteins?

A

Pancreatic proteases cleave proteins after specific amino acid residues

Trypsin: - after Arg or Lys residues.
Chymotrypsin: - after bulky and aromatic residues.
Elastase: - after Gly, Ala, Ser residues.
Carboxypeptidases A or B (exo-peptidases) cleave amino acids from
the carboxyl-end.

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11
Q

What pancreatic proteases ends the. Cascade?

A

The different proteases act simultaneously
on the same proteins. Carboxypeptidases finish the job.

The digestive proteases cleave the dietary proteins. After dietary proteins
are cleaved the pancreatic proteases cleave the digestive enzymes.
This leads to an uptake of more amino acids than provided by the diet

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12
Q

Summarize the absorption of amino acids

A

The uptake of dietary amino acids is mainly performed by secondary active transport with cotransport of sodium ions.

The transporters are specific for a group of amino acids which can be overlapping.

The release into the portal vein is by facilitated transpor

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13
Q

Summarize the big picture of carbohydrate digestion and absorption

A
  1. Mouth: salivary a-amylase degrades starch and glycogen to dextrins, isomaltose and maltose.
    Humans cannot digest cellulose (lost in feces).
  2. Stomach: carbohydrate digestion stops.
  3. Small intestine: pancreatic a-amylase forms isomaltose and maltose.
  4. Brush border cells: disaccharidases cleave lactose, sucrose, isomaltose and maltose.
  5. Intestinal mucosal cells: release of glucose, fructose and galactose into the portal
    vein for transport to the liver
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14
Q

Describe the absorption of dietary monosaccharides

A

Dietary fructose enters the intestinal mucosal
cells via facilitated transport by GLUT-5.

Dietary glucose and galactose
enter the intestinal mucosal cells via SGLT-1 which uses a secondary active transport and cotransport with sodium ions.

All three monosaccharides
are released by facilitated transport by GLUT-2 into the portal vein.

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15
Q

Summarize lipid digestion and absorption

A
  1. Mouth: lingual lipase is mainly swallowed.
  2. Stomach: lingual and gastric lipase degrade milk TAGs
    with medium-chain FA.
  3. Small intestine: Bile is needed for lipid degradation
    and absorption.
  4. Brush border cells: uptake of free fatty acids, MAG, free cholesterol and lipid-soluble
    vitamins needs mixed micelles with bile salts.
  5. Intestinal mucosal cells: TAGs and cholesteryl esters are formed and dietary lipids are released into the lymph inside of chylomicrons.
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16
Q

What is bile?

A

Bile is an alkaline fluid
that is released by hepatocytes into the bile ducts.

Bile contains: bile salts, phosphatidylcholine, free cholesterol and other.
Bile can be stored and concentrated in the gall bladder

17
Q

What are the functions of bile?

A
  1. Transportation of free cholesterol and conjugated bilirubin in the bile from the liver to the duodenum. Bile salts increase solubility of free cholesterol in bile.
  2. Emulsification of dietary lipids in the small intestine for digestion by pancreatic lipase and cholesteryl esterase.
  3. Uptake of digested lipids into intestinal mucosal cells by forming mixed micelles.
18
Q

What is the purpose of pancreatic lipase?

A

The protein colipase pushes the bile salts
away from TAGs and anchors pancreatic lipase to the lipid droplet.

The purpose of pancreatic lipase is to form molecules that can enter the intestinal mucosal cells.

This is achieved with MAGs which are not further degraded.

19
Q

What is the clinical aaplication of pancreatic lipase?

A

Pancreatic lipase is inhibited by the drug Orlistat which is used for weight loss treatment

20
Q

Summarize special TAG synthesis in mucosal cells

A

Only intestinal mucosal cells can start TAG synthesis with MAG formed by pancreatic lipase.

This special MAG pathway of TAG synthesis uses dietary MAG and fatty acids

21
Q

What is the fate of chylomicrons?

A

Chylomicrons filled with dietary lipids are released into the lymph and reach the blood.

The dietary TAGs in chylomicrons are cleaved by lipoprotein lipases (LPL) mostly in capillaries of the heart and fat cells. The formed fatty acids are used for energy metabolism in heart and muscle or
are stored in fat cells as TAGs.

Only the chylomicron remnants containing less TAGs, mainly cholesteryl ester and the lipid-soluble vitamins are taken up by the liver by endocytosis.

22
Q

Describe the enterogepatic circulation of bile salts

A

Hepatocytes release bile salts into bile canaliculi and the bile reaches the duodenum.

Bile salts are needed for:
1. Cholesterol transport into duodenum.
2. Emulsification for digestion and
3. Absorption of dietary lipids in the duodenum,
jejunum and ileum.

95% of bile acids/salts are reabsorbed at the terminal ileum and reach the liver via the hepatic portal vein. They are transported in the blood bound to albumin.
The normal bile salt pool is about 3-5 g and about
0.5 g of bile acids/salts are lost per day into feces

23
Q

What is enterohepatic circulation?

A

The enterohepatic circulation describes the formation of bile salts in the liver, their release into the bile ducts, the eventual reabsorption of bile salts/acids from the intestine and finally their transport back into the liver via the portal vein

24
Q
A

The liver conjugates primary and secondary bile acids with glycine or taurine and releases bile salts and free cholesterol into the bile. Bile reaches the duodenum and the bile salts are now used for emulsification of dietary lipids mainly in the duodenum, jejunum and ileum. Bacteria from the large intestine are present in the terminal ileum and deconjugate bile salts to bile acids and glycine or taurine. Some primary bile acids are modified by these intestinal bacteria to secondary bile acids. A mixture of primary and secondary bile acids is taken up and reach the liver via the portal circulation. Hepatocytes conjugate primary and secondary bile acids for another cycle of the enterohepatic circulation. Only 5% of the released bile salts are excreted in feces

The small loss of bile acids is refilled in the liver by synthesis of primary bile acids using free cholesterol

25
Q

Why are bile salts important for cholesterol metabolism?

A

Bile salts are important for cholesterol metabolism:
1. Bile salts increase the solubility of free cholesterol in bile and allow transport of cholesterol into the intestine for release in feces.

  1. Cholesterol is used for synthesis of bile acids and the lost bile acids in feces need to be refilled by bile acid synthesis using cholester
26
Q

What are the main functions of bile salts?

A
  1. Transport of free cholesterol from the liver into the duodenum for eventual release of free cholesterol in feces.
  2. Emulsification of dietary lipids in the small intestine needed
    for pancreatic lipase, cholesteryl esterase and PLA2.
  3. Formation of mixed micelles for uptake of dietary lipids into the intestinal mucosal cells.
  4. Usage of free cholesterol in hepatocytes for synthesis of
    primary bile acids after release of 5% of bile salts into feces
27
Q

What are the possible causes of steatorrhea?

A
  1. Lack of bile salts due to:
    Liver damage including liver cirrhosis. Bile duct obstruction by gallstones. Pancreatic tumor.
  2. Defects related to pancreatic juice:
    Deficiency of enzymes:
    - Lack of transport into the intestines in CF. - Lack of bicarbonate secretion which
    impairs the adjustment of the pH in the duodenum.
  3. Defective intestinal mucosal cells or shortened bow
28
Q

What causes cholelithiasis?

A

Cholesterol gallstone disease can be caused by
• Reduction of hepatic bile salt secretion and imbalance with free
cholesterol release.

• Increased biliary free cholesterol secretion leads to less solubility of
cholesterol creating cholesterol gallstones.

Bile duct obstruction impairs dietary lipid digestion as bile salts do not reach the small intestine resulting in:

  • Less emulsification of lipids.
  • Less uptake of digested lipids
29
Q

How can gallstones lead to pancreatitis?

A

Gallstones can block the pancreatic duct preventing the zymogens to be released into the duodenum causing pancreatitis.

Trypsin is pre-maturely active in the pancreas activating other pancreatic zymogens which can destroy proteins and the phospholipid membranes.

The pancreatic enzymes are not secreted into the duodenum which diminishes the digestion of all food groups

30
Q

Explain the impact of cystic fibrosis of the pancreas

A

Patients with cystic fibrosis (CF) have a deficiency of CFTR which leads to less
release of chloride ions and water.

Mucus and protein plugs block the pancreatic duct. Less pancreatic zymogens and enzymes reach the duodenum. Digestion of proteins and lipids is mainly reduced, whereas amylase is still active at low enzyme concentrations.

CF patients often have chronic pancreatitis, steatorrhea and are undernourished.

Dietary treatment with carbohydrates and TAGs with medium-chain fatty acids which
are already cleaved in the stomach. The formed medium-chain fatty acids reach directly the liver.

31
Q

Summarize The characteristics of hormone sensitive lipase

A

Made in adipocytes

Active in Same adipocytes that synthesize this hormone sensitive lipase

Purpose: Hormonal control of the degradation of TAGs stored in fat cells and release of free fatty acids and glycerol into the blood during fasting and fight or flight situations (epinephrine).

32
Q

Summarize lipoprotein lipases

A

Synthesized in Myocytes, adipocytes and other

Active in the Blood where the lipase is anchored in capillaries of heart, muscle and fat tissue. Need apo CII for activation

Purpose: Cleavage of TAGs in chylomicrons and VLDLs which provides free fatty acids for uptake into heart and muscle (energy metabolism) or into fat cells for synthesis and storage of TAGs.

33
Q

Summarize the characteristics of pancreatic lipase

A

Synthesized in Acinar cells of exocrine pancreas

Active in the Intestinal lumen which needs bile salts for emulsification of dietary TAGs and colipase for anchoring to TAGs

Purpose: Cleavage of TAGs to MAGs for uptake into intestinal mucosal cells. Provision of the substrate for the specific MAG pathway for TAG synthesis in intestinal mucosal cells.

34
Q

Summarize the characteristics of gastric and lingual lipase

A

Synthesized in:
Salivary gland cells Gastric chief cells

Active in the:
Stomach lumen Acid-stable enzymes Need low pH

Purpose:
Degradation of TAGs with medium- chain fatty acids (milk). Important for babies and patients with CF. No bile salts neede

Digestion And Metabolism (57 decks)

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