Nutrient Absorption Flashcards
1
Q
salivary enzymes
A
-amylase and lingual lipase
2
Q
stomach enzymes
A
- gastric chief cells secrete pepsinogen-pepsin at low pH
- endopeptidase for aromatic L aa
- optimum pH 1-3, inactive at 5
- gastric lipase
3
Q
pancreatic enzymes
A
- amylase
- endopeptidases-trypsin, chymotrypsin, elastase
- exopeptidases (carboxypeptidase)
- lipase/colipase
- phospholipase A2
- cholesterol esterase
4
Q
intestinal extoenzymes
A
- membrane bound in brush border, catalytic site faces lumen
- enterokinase-activates trypsin
- disaccharideases
- peptidases
5
Q
activation of pancreatic proteolytic enzymes
A
- enterokinase activates trypsin from trypsinogen
- trypsin then activates chymotrypsin, eslastase, and carboxypeptidase A and B
- the carboxy are exopeptidases, others are endo
6
Q
protein digestion and absorption of peptides/aa
A
- proteins yield 40% aa and 60% oligopeptides (2-6)
- single aa carried across via a Na cotransporter
- up to tetra peptides-cleaved by brush border peptidases or pumped across with a H+ cotransporter
- then cleaved by teta/tri/di peptidases inside cell and diffuse out into cap
- newborns can absorb globulins and other whole proteins, allergies to some foods can be whole protein absorption
7
Q
sterospecific absorption
A
- more L form absorbed that D form
- absorption is sterospecific
- therefore it’s not just diffusion
8
Q
uptake by hamster intestine
A
- absorption is against a gradient
- everted sacs and aa concentrated against gradient
9
Q
Na coupled aa transport
A
- aa require inward sodium gradient for (out to in) concentrative uptake
- increasing Na led to increased aa uptake
- pump Na out and K in on baso-lateral
- Na and aa co-transport in on apical membrane
10
Q
transport kinetics
A
- vmax and km
- the transporters in the membrane become saturated
- MM kinetics
- free diffusion would be linear
11
Q
brush border membrane
A
- see table- too hard to compact here
- slide 9
12
Q
H/oligo transporter
A
- PepT1
- di/tri/tetra peptides into enterocyte
13
Q
hartnup disease
A
- can’t uptake phenylalanine
- can take phenyylalanyl and leucine, and arginine and cysteine
- system B is defective
- high tryptophan in urine because affects kidney too
14
Q
cystinuria
A
- system B0+ affected
- can’t uptake arginine or cysteine
- basic aa absorption reduced
- forms kidney stones
15
Q
digestion and absorption of sugars
A
- brush border extoenzymes convert maltose (glu-glu), lactose (glu-gal) and sucrose (glu-fru) to monosaccharides
- carbs absorbed as simple sugars
- Glu and gal compete for same Na coupled carrier
- fructose is independent of Na and cannot be concentrated in cell
- ingested carb is 60% starch, 30% sucrose, 10% lactose
- salivary amylase begins digestion
- ptyalin has pH optimum of 6.7 and is inactivated in stomach
- most starch broken down in intestine by pancreatic amylase
- transport is facilitated diffusion of Na coupled
- SGLT1 is Na coupled transporter for glu or gal
- GLUT 5 mediates diffusion of fructose
- GLUT2 mediates diffusion out
16
Q
undigested fiber
A
- no cellulase for digesting cellulose of hemi-cellulose
- maintains consistency of stool
17
Q
lactose intolerance
A
- lactose is osmotically active, osmotic diarrhea
- lactaid is milk containing lactase
- lactose tolerance test- give oral load, measure blood glu
- lactose deficiency will have more H2 breathed out and won’t ingest as much lactose, less lactose to glucose
- bacteria in gut ferment lactose and make lots of gas
18
Q
glucose/galactose malabsorption
A
- rare genetic disease
- SGLT1 carriers are missing or defective
- accumulation of glu in intestine causes diarrhea, dehydration, and death
- patients die soon after birth if diarrhea isn’t diagnosed
- restricted diet of fructose
19
Q
fats
A
- neutral fat
- phospholipids
- cholesterol
- fatty acids
- waxes of ingested plant cell walls
20
Q
CCK
A
- fats cause release
- GIP decreases gastric acid secretion
- CCK:
- slows gastric motility and emptying, stimulates pancreatic enzyme secretion
- stimulates intestinal fluid secretion
- stimulates gallbladder contraction
- relaxes sphincter of Oddi
21
Q
digestion of fats
A
- starts with lingual lipase
- continues with gastric lipase and food-bearing lipase with acidic pH optima
- digestion occurs mostly in the jejunum and is completed by the mid jejunum via:
- pancreatic phospholipase A2, cholesterol esterase, pancreatic lipase
22
Q
fat globules and micelles
A
- micelles have long chain FA
- cholesterol
- monoglycerides
- phospholipids
- bile salts
- fat soluble vitamins
- mixed with amphipathic bile salts
- lipases hydrolyze TAGs at surface, core replaces them and they shrink
23
Q
absorption of neutral fat
A
- mixed micelles carry major part of lipids, once they diffuse, emulsifying more lipids recycles empty bile micelle, bile salt doesn’t diffuse in
- FA with short chain are more hydrophilic, diffuse directly
- for long chain-need FATP takes them to sER to re-esterification
- NPC1L1 is a transporter for cholesterol
- bile salts not absorbed in jejunum, in ileum into portal system for recycling- can be reused even in a single meal
24
Q
formation of chylomicrons
A
- LCFA and other products of lipid digestion are converted back to triglycerides, phospholipids, and esters of cholesterol in SER
- fat droplets form in the cisternae of the SER
- apoproteins are synthesized in RER and transferred to the SER, where they associated with lipid droplets
- nascent chylos and VLDLs arrive at the cis face of the Golgi apparatus, apoproteins are glycosylated
- vesicles carrying chylos or VLDLs bud off from the trans golgi, move to the basolateral membrane in transport vesicles
- vesicles fuse with the basolateral membrane and release chylos or VLDLs
- chylos and VLDLs pass through large interendothelial channels of lymphatic capillaries and enter lymph
- glycerol, SCFA, MCFA pass through enterocyte and enter blood cap
