GI Phys Lecture 3

Question 1

Hepatocytes synthesize ______. How are each reabsorbed?

Answer 1

Bile acids, only primary.

Hepatocytes synthesize primary bile acids from cholesterol which can be modified which changes solubility. Reabsorbed actively.

Secondary bile acids reabsorbed passively, formed from primary bile acids.

Question 2

Fat soluble vs water soluble

Answer 2

Fat soluble can be reabsorbed anywhere. If it is more water soluble, requires certain transporter.

Question 3

Primary bile acids location and how are they reabsorbed / produced

Secondary bile acid location and how are they reabsorbed / produced

Answer 3

Primary: Reabsorbed actively in ileum, requires co-transport with Na+. produced by liver

Secondary: Reabsorbed passively throughout intestines. More lipid soluble. produced by bacteria

Question 4

What drives bile acid cycle?

Answer 4

Your diet. How much / how frequent you eat. Bile acids have something to do with fat in diet.

Question 5

Recycling of bile acids.

Answer 5

as food moves along , it gets mixed with pancreatic secretions for examples, and along with bile acids. Lose some bile acids, only synthesize amount we lose. Otherwise we recycle bile acids

If secondary bile acid by portal circulation comes back to hepatocytes, hepatocyte has to make a modification. Hepatocytes convert secondary bile to primary ones.

Question 6

Gallbladder Function:

Where does bile travel and in response to what?

What stimulates gallbladder contractions?

Answer 6

Gallbladder accumulates bile while fasting.

In response to fats / protein digestion in duodenum, bile passes through common bile duct -> Oddi’s sphincter (where pancreatic duct enters too) and goes into duodenum in spurts.

CCK and ACh stimulate gallbladder contractions via smooth muscle contractions

Question 7

Neurotransmitters that relax Oddi’s Sphincter

Answer 7

VIP / NO

When sphincters close, bile will accumulate in gallbladder, and you reabsorb water and concentrate contents of bile.

Question 8

Causes of Gallstones

Answer 8

Too much absorption of water from bile
Too much absorption of bile acids from bile
Too much cholesterol in bile
Inflammation of epithelium

Question 9

transcellular process

Answer 9

From unstirred layer, through microvilli, through basolateral membrane

Brush border: unstirred layer / microvilli

Question 10

Cell cycle of enterocytes.

Answer 10

Mitosis in crypt, cell migration and maturation. they differentiate here, cell death on tip of villus, slough off.

Question 11

intestinal absorption of water

Transcellular

Answer 11

Transporters moving sodium from lumen into cell. then leaves and goes into interstitial space. Water follows sodium.

Absorption of water linked by SGLT-1

Question 12

Intestinal absorption of water

Paracellular

Answer 12

Tight junctions contain claudins, aquaporins present within claudins

Accumulation of ions in interstitial spaces create osmotic gradient

Question 13

Absorption in small intestine:

Na+ cotransported with what?

Answer 13

Glucose , AAs

Question 14

Absorption in small intestine:

Cl- absorbed how?

Answer 14

Paracellularly (between enterocytes) through channels

Question 15

Absorption in small intestine:

Ca2+ absorbed how?

Answer 15

Passively and actively. Active absorption facilitated by vitamin D.

Question 16

Absorption in small intestine:

Mg2+ absorbed where?

Answer 16

Ileum, actively

Question 17

Absorption in small intestine:

Fe3+ absorbed in what form? What is the mechanism?

Answer 17

as Fe2+ (ferrous iron) as heme. Cannot absorb when it is Fe3+, therefore iron reductase makes it into Fe2+.

Mechanism: Fe2+ cotransported with H+ in apical membrane. Then binds to Ferritin bc it is toxic by itself.

Heme gets transported via HCP1 (heme carrier protein) and once internalized, it is broken down into iron and transported out same way. CO and Biliverdin = byproducts.

Question 18

Absorption in small intestine:

Vitamin C and B12 absorbed where?

Answer 18

Ileum, actively

Question 19

Digestion / Absorption of Dietary Carbohydrates:

How does glucose, maltose, a-dextrin, lactose, sucrose, fructose, galactose get into enterocyte?

Answer 19

Glucose, galactose, fructose go directly into enterocyte. Glucose / galactose absorbed in cotransport with Na+ via SGLT-1. Fructose via ___.

Sucrose -> fructose / glucose via sucrase

Lactose -> galactose / glucose via lactase

Maltose -> glucose via maltase

a-Dextrin -> glucose via isomaltase

Note: Starch yields a-dextrin and maltose via salivary amylase / pancreatic amylase.

Question 20

Digestion / Absorption of Dietary Proteins

Mechanism

Answer 20

1.) Proteases hydrolyze proteins to oligopeptides / single AAs

2.) Apical membrane peptidases convert oligopeptides -> di / tri-peptides and free AAs, which can either convert to AAs or go into enterocyte

3.) Single AAs absorbed into portal blood. Requires several specific enterocyte apical / basolateral transporters.

Question 21

Digestion / Absorption of Dietary Lipids

Mechanism

Answer 21

1.) Dietary fat stimulates CCK, CCK stimulates pancreatic lipase.
2.) Lipase hydrolyzes triglycerides -> LCFAs -> mixed micelles (contain bile salts)
3.) Micelles enter enterocytes, re-esterified into triglycerides
4.) Triglycerides incorporated into chylomicrons (no bile salts). Enter lymph capillaries.
5.) Vitamins ADEK are in mixed micelles and chylomicrons.

Question 22

How do we avoid overload of good bacteria?

skip

Answer 22

Migrating motor complexes associated with fasting, triggered by motilin.

Question 23

Consequences of Bacterial overgrowth

skip

Answer 23

Fermentation

B12 deficiency (bacteria competes with body for B12)

Increased secondary forms bile acids from primary. This is a problem because for maximum lipid absorption, we need primary bile acids to be absorbed in ileum, not sooner. Secondary absorbs sooner.