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Flashcards in Digestion and Absorption Deck (28)
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1

describe digestion in the mouth

  • starts with carbohydrate digestion by the enzyme salivary α-amylase that cleaves α1-4 glycosidic bonds of starch and glycogen and it forms branched oligosaccharides
  • lingual lipase for ipid digestion is released in the oral cavity but is mainly swallowed

2

describe the purpose of HCl

  • HCl denatures food for quicker digestion and also destroys pathogens
  • HCl alters the conformation of pepsinogen in order for it to cleave itself, producing the active protease pepsin (autocatalytic activation)
    • pepsin is an endopeptidase and cleaves peptide bonds within a protein chain
    • pepsin has a optimum pH of 2

3

describe the digestion in the stomach

  • carb digestion stopped due to denatured salivary α-amylase
  • protein and lipid digesiton start in the stomach due to acid-stable enzymes 
  • pepsin degrades proteins to large peptides
  • lingual and gastric lipases degrade TAGs with medium-chain FAs (long chain FA degraded later)
    • medium-chain FAs go directly to the liver and available for energy metabolism 
    • does not need bile salts/pancreatic enzymes

4

describe the purpose of secretin and CCK

  • released from endocrine cells of the duodenum when the acidic chyme reaches 
  • secretin leads to secretion of bicarb and water from the pancreas
    • bicarb used to change the acidic pH to a neutral pH in duodenum
  • CCK leads to release of pancreatic enzymes and bile into the duodenum

5

describe cholecystokinin

  • activates release of bile from gallbladder
  • inhibits gastric motility which allows neutralization of the acidic chyme that entered the duodenum
  • activates enteropeptidase in the duodenum
  • activates secretion of pancreatic enzymes, zymogens ad proteins

6

describe the activation of pancreatic zymogens

  • trypsinogen is released by the pancreas and is activated to trypsin after it reaches the lumen of the duodenum
    • this separation prevents pancreatic damage since trypsin is a powerful protease that activates all other pancreatic zymogens

7

what does trypsin activate?

  • zymogens to active enzymes
  • proenzymes to active enzymes
  • lipid digestion:
    • procolipase to colipase (protein, not an enzyme)
    • prophospholipase A2 to phospholipase A2

8

describe where in the sequence pancreatic proteases cleave proteins

  • trypsin: cleaves after arg/lys residues
  • chymotrypsin: cleaves after bulky/aromatic residues
  • elastase: cleaves after glycine, alanine, serine residues
  • carboxypeptidase A or B (exopeptidases) cleave amino acids from the carboxyl-end

9

which pancreatic enzymes are cleaved after dietary proteins are digested?

  • pancreatic lipase
  • pancreatic α-amylase
  • pancreatic phospholipase A2

 

  • all formed amino acids are taken up into the intestinal mucosal cells
  • the final uptake of amino acids is larger than the intake of dietary amino acids (dietary AAs + digestive AAs)

10

describe the absorption of dietary amino acids

  • the uptake of dietary amino acids is performed by secondary active transport with cotransport of sodium ions
  • the trasporters are specific for a group of amino acids which can be overlapping
  • the release into the portal vein is by facilitated transport

11

describe the big picture of digestion and absorption of carbs

12

describe the oligo- and disaccharide digestion by brush border enzymes

13

describe carb digestion in the small intestine

  • pancreatic α-amylase acts on polysaccharides and oligosaccharides (which were formed in the mouth by salivary α-amylase) to generate: maltose, isomaltose and some small oligo-saccharides (dextrin)
    • these sugars are finally degraded to glucose by the sucrase-isomaltase complex as well as by maltase-glucoamylase
  • enzymatic degradation of dietary disaccharides:
    • sucrase degrades sucrose to glucose and fructose
    • lactase degrades lactose to glucose and galactose 

14

describe lactose intolerance

  • lactose intolerant individuals cannot properly digest lactose in the small intestine and lactose passes into the large intestine
  • bacteria degrade lactose to osmotically active compounds resulting in large volumes of hydrogen has and CO2 which causes abdominal cramps, diarrhea and flatulence
    • the osmotic diarrhea results from water coming from the mucosal cells that enters the lumen of the large intestine

15

describe congenital lactase deficiency

  • lactase activity is normally the highest after birth
  • congenital lactase deficiency leads to severe osmotic diarrhea and dehydration in the baby
    • the baby cries due to painful bloating 
  • these neonates need lactose-free formula

16

describe primary lactose intolerance

  • the amount of lactase is strongly reduced (this is normal) at about 7 years of age in the majority of humans

17

describe secondary lactose intolerance

  • can occur due to loss or damage of intestinal mucosal cells (food poisoning)
  • severe diarrhea or gastroenteritis due to rotavirus can lead to intestinal injury
  • Celiac disease is immune-mediated causing damage to the intestinal mucosa in response to gluten (protein in grains)

18

describe the absorption of dietary sugars

  • the absorption of dietary glucose and galactose is performed by SGLT-1
    • SGLT-1 uses secondary active transport and cotransport with Na ions
  • dietary fructose enters the intestinal mucosal cells via facilitated transport by GLUT-5
  • all 3 monosaccharides are released by facilitated transport by GLUT-2 into the portal vein

19

describe the big picture of DNA and RNA digestion and absorption

20

describe the overview of lipids

21

describe the main functions of bile

  • transport of free cholesterol and conjugated bilirubin from the liver into the duodenum for eventual release of free cholesterol in feces
  • delivery of conjugated bile salts and phosphotidylcholine to the small intestine for emulsification of dietary lipids for digestion
  • formation of mixed micelles for uptake of dietary lipids into the intestinal mucosal cells
  • release of 5% of bile salts into feces 

22

contrast bile acids and bile salts

  • 2 differences:
    • A negative charge is needed for the hepatic ABC transporter
      • the conjugation of bile acids with glycine or taurine changes the pKa to 4 or 2, respectively
    • improves emulsification of dietary fat in the intestines

23

explain the difference between a primary and secondary bile acid

  • primary bile acids are synthesized only in the liver which uses free cholesterol 
    • cholic acid
    • chenodeoxycholic acid
  • secondary bile acids are formed by modification of primary bile acids by bacteria in the ileum
    • deoxycholic acid
    • lithocholic acid

24

list the steps of bile production process in the liver

  • synthesizes primary bile acids from free cholesterol (cholesterol 7-α-hydroxylase)
  • conjugates primary or secondary bile acids with glycine or taurine
  • releases conjugated bile salts and free cholesterol into the bile canaliculi via the ABC-transporter

25

describe pancreatic lipase

  • pancreatic lipase is secreted with procolipase by the pancreas and reaches the duodenum
    • procolipase is cleaved to colipase in the duodenum by trypsin
  • digestion of dietary triacylglycerols by pancreatic lipase needs release of bile salts stimulated by CCK
  • pancreatic lipase is not synthesized as a zymogen
    • it cannot act in the healthy pancreatic cells since the substrate (TAGs), bile salts and colipase are not present 

26

the special _____ pathway of _____ synthesis is found in ______ cells

the special MAG pathway of TAG synthesis is found in intestinal mucuosal cells

  • pancreatic lipase forms MAG and 2 fatty acyl CoAs which can be directly linked to form TAGs
  • TAGs and cholesteryl ester and lipid soluble vitamins are released inside of chylomicrons into the lymph

27

describe the fate of chylomicrons in the body

28

describe 3 possible causes of steatorrhea

  • lack of conjugated bile salts
    • due to liver damage including liver cirrhosis or bile duct obstruction by gallstones or tumor
  • defects related to pancreatic juice
    • deficiency of enzymes, lack of transport of enzymes into the intestines like seen in CF or lack of bicarb secretion which would impair pH adjustment in duodenum
  • defective mucosal cells related to uptake of nutrients
    • a shortened bowel could also lead to steatorrhea