GI Phys Lecture 3 Flashcards
Hepatocytes synthesize ______. How are each reabsorbed?
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.
Fat soluble vs water soluble
Fat soluble can be reabsorbed anywhere. If it is more water soluble, requires certain transporter.
Primary bile acids location and how are they reabsorbed / produced
Secondary bile acid location and how are they reabsorbed / produced
Primary: Reabsorbed actively in ileum, requires co-transport with Na+. produced by liver
Secondary: Reabsorbed passively throughout intestines. More lipid soluble. produced by bacteria
What drives bile acid cycle?
Your diet. How much / how frequent you eat. Bile acids have something to do with fat in diet.
Recycling of bile acids.
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.
Gallbladder Function:
Where does bile travel and in response to what?
What stimulates gallbladder contractions?
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
Neurotransmitters that relax Oddi’s Sphincter
VIP / NO
When sphincters close, bile will accumulate in gallbladder, and you reabsorb water and concentrate contents of bile.
Causes of Gallstones
Too much absorption of water from bile
Too much absorption of bile acids from bile
Too much cholesterol in bile
Inflammation of epithelium
transcellular process
From unstirred layer, through microvilli, through basolateral membrane
Brush border: unstirred layer / microvilli
Cell cycle of enterocytes.
Mitosis in crypt, cell migration and maturation. they differentiate here, cell death on tip of villus, slough off.
intestinal absorption of water
Transcellular
Transporters moving sodium from lumen into cell. then leaves and goes into interstitial space. Water follows sodium.
Absorption of water linked by SGLT-1
Intestinal absorption of water
Paracellular
Tight junctions contain claudins, aquaporins present within claudins
Accumulation of ions in interstitial spaces create osmotic gradient
Absorption in small intestine:
Na+ cotransported with what?
Glucose , AAs
Absorption in small intestine:
Cl- absorbed how?
Paracellularly (between enterocytes) through channels
Absorption in small intestine:
Ca2+ absorbed how?
Passively and actively. Active absorption facilitated by vitamin D.
Absorption in small intestine:
Mg2+ absorbed where?
Ileum, actively
Absorption in small intestine:
Fe3+ absorbed in what form? What is the mechanism?
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.
Absorption in small intestine:
Vitamin C and B12 absorbed where?
Ileum, actively
Digestion / Absorption of Dietary Carbohydrates:
How does glucose, maltose, a-dextrin, lactose, sucrose, fructose, galactose get into enterocyte?
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.
Digestion / Absorption of Dietary Proteins
Mechanism
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.
Digestion / Absorption of Dietary Lipids
Mechanism
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.
How do we avoid overload of good bacteria?
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Migrating motor complexes associated with fasting, triggered by motilin.
Consequences of Bacterial overgrowth
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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.
