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102 Cards in this Set

  • Front
  • Back

most diestion occurs in

the small intestine (duodenum, jejunum) and is complete by the ileum

functional reserve for digestion

surplus of digestive enzymes are present

functional reserve for absorption

surplus of transporters is present

macronutrients

CHO, protein, fat

micronutrients

minerals that are required in greater quantity than trace-elements

2 major types of enzymes for digestion

luminal or cavity digestion is due to enzymes secreted from salivary glands, stomach, and pancreas into the lumen; membrane or contact digestion is due to enzymes bound to the apical microvillar membrane of intestinal enterocytes

what are not necessary for complete digestion

salivary and gastric luminal enzymes

all luminal digestion can be accomplished by

pancreatic enzymes

malnutrition occurs with

90% loss of pancreatic enzymes

normally pancreatic enzymes are responsible for what percent of digestion

50% of carbohydrate digestion; 50% of protein digestion; 90% of lipid digestion

all membrane or contact digestion occurs in

the small intestine

adaptation- pancreatic enzyme expression responds to

long term changes in diet

size of the segments of the small intestine

duodenum 1-2 feet, jejunum 8 ft, ileum 12 feet

size of large intestine

5 feet

absorption occurs at

villi; villi are made of many cells; microvilli are microscopic cellular membrane protrusions that increase the surface area of individual cells

functional hyperemia within the intestine allows for

local control of blood flow

what primarily enter the blood supplu

hydrophilic nutrients, ions, and H2O

where does fat absorb

digestion products primarily enter the lymphatic lacteals

blood flow in each area of GIT/layer of the gut wall is directly related to

the level of local activity (during active absorption of nutrients- increases 8 fold)

causes of increased blood flow

endocine agents that act as vasodilators (CCK, VIP, gastrin, secretin); GI gland vasodilators- kinins (most powerful), kallidin, and bradykinin; reactive hyperemeia from tissue hypoxia under normal conditions of digestion including release of adenosine

countercurrent blood flow at the villi results in

O2 diffusing from arteries into veins such that O2 tension at tips of villi is lowered; in circulatory shock the O2 deficit in the tups of the villi can become so great that the villus tip or event he whole villus suffers ischemic death

sympathetic vasoconstriction of intestinal and mesenteric veins can provide

200-400 mL of extra blood (e.g. hemorrhagic shock)

dietary carbohydrates

50% of caloric intake or 1200-2000 calories/day; polysaccharides, disaccharides and oligosaccharides, monosaccharides

steps in the digestion of carbohydrates

luminal digestion of polysaccharides (plant starch and animal starch (glycogen)) --> membrane digestion of disaccharides and oligosaccharides --> absorption of monosaccharides by enterocytes; membrane digestion occurs on villi of brush border in small intestine

salivary and pancreatic alpha amylase cleage of

interior 1,4-glycosidic bonds of hydrolysis; for absorption dietary carbohydrates must be broken down into monosaccharides

trehalose contains

1,1 glycoside bond between 2 alpha-glucose units

lactose (milk sugar) is

a disaccharide that consists of beta-D-galactose and beta-D- glucose

sucrose consists of

2 monosaccharides, alpha glucose and fructose, joined by a glycosidic bond between carbon atom 1 of the glucose unit and carbon atom 2 of the fructose unit

dextrins are

a group of low molecular weight carbohydrates produced by the hydrolysis of starch; they are mixtures of linear alpha-(1,4)-linked D-glucose polymers starting with an alpha-(1,6) bond

saliva- active enzyme, substrate acted upon, product

alpha amylase; plant starch and glycogen are broken down into alpha limit dextrins, maltose, and maltotriose

pancreatic juice- active enzyme, substrate acted upon and product

alpha amylase; plant starch and glycogen into alpha limit dextrins, maltose, and maltotriose

intestine juice- active enzymes, substrates acted upon and product

alpha dextrinase breaks down alpha limit dextrins into glucose; glucoamulase breaks down maltooligosaccharides (e.g. maltotriose) into glucose; maltase breaks down maltose into glucose; sucrase breaks down maltotriose and sucrose into fructose and glucose; lactase breaks down lactose into galactose and glucose

lactose intolerance

the inability to metabolize lactose because lactase is absent or its availability is lowered; 75% of adults worldwide show some decrease in lactase activity; breath H2 test for lactose intolerance; for lactose intolerance substitute dietary sucrose

lactose hydrogen breath test

give them lactose and measure H+ in the breath; it it is there then they can't break down lactose

cellulose versus starch

difference is that cellulose is a beta-1,4-linked glucose polymer while starch is an alpha-1,4 linked glucose polymer; human intestinal enzymes cannot hydrolyze beta glycosidic linkages; cellulose and other molecules with beta-glycosidic linkages contribute to dietary fiber; termites and herbivores use microbial digestion of cellulose; enzymes are important in the breakdown of these 2 molecules into simpler sugars which can serve as energy sources; the enzymes that break down starch are called amylases and those that break down cellulose are cellulases; humans have amylases but lack cellulases; bacteria make cellulases and animals that have a lot of bacteria in their guts like cows and termites can digest cellulose; that is why celery is so low calorie and potatoes aren't

absorption of carbohydrates- SGLT1

electrogenic; secondary active transport

absorption of carbohydrates- what is transported at the brush border

monosaccharides

3 main end products of carbohydrate digestion

glucose, galactose, and fructose

what has the highest capacity to absorb monosaccharides

the duodenum and upper jejunum

5-15% of CHO passes undigested to the colon where it is

metabolized by colonic epithelial cells

3 main sources of fructose

sucrose (common table sugar), high fructose corn syrup (HFCS) made from corn starch, and fruits; one of the largest cources of fructose is sugar sweetened beverages

GLUT5 is a

specific fructose transporter

fructose malabsorption or dietary fructose intolerance is

a dietary disability of the small intestine where the amount of fructose carrier in enterocytes is deficient

digestion of carbohydrates to monosaccharifes

salivary and pancreatic alpha are endoenzymes; they can digest the linear internal alpha-1,4 linkages between glucose residues but they cannot break terminal alpha-1,4 linkages (i.e. between the last 2 sugars in the chain); they also cannot split the alpha-1,6 linkages at the branch points of amylopectin or the adjacent alpha 1,4 linkages; as a result the products of alpha amylase are linear glucose oligomers, maltotriose (a linear glucose trimer), altose (a linear glucose dimer), and alpha limit dextrins (which contain an alpha-1,6 branching linkage); the brush border oligosaccharidases are intrinsic membrane proteins with their catalytic domains facing the lumen; the sucrase isomaltase is actually 2 enzymes and therefore 4 oligosaccharidases split the oligosaccharides produced by alpha amylase into monosaccharides; SGLT1 IS THE Na+ COUPLED TRANSPORTER THAT MEDIATES THE UPTAKE OF GLUCOSE OR GALACTOSE FROM THE LUMEN OF THE SMALL INTESTINE INTO THE ENTEROCYTE; GLUT5 MEDIATES THE UPTAKE OF FRUCTOSE FROM THE LUMEN OF THE SMALL INTESTINE INTO THE ENTEROCYTE; GLUT2 MEDIATES THEIR EFFLUX ACROSS THE BASOLATERAL MEMBRANE INTO THE INTERSTITIAL SPACE (THESE THREE ARE CONTACT ENZYMES)

protein sources

diet, GI secretions, GI cells

dietary protein digestion and absorption are normally completed in

the small intestine

protein in feces (desquamated cells, bacteria, mucus) is primarily of what origin

colonic

what is the requirement of protein

350-500 g/day versus 300-500 g/day of carbohydrates

steps in the digestion of proteins

luminal digestion of proteins by proteases --> membrane digestion of polypeptides by peptidases --> TRANSPORT OF TRI-, DIPEPTIDES, AND INDIVIDUAL AMINO ACIDS ACROSS ENTEROCYTE BRUSH BORDER (this is a big difference from the carbs that we can only absorb as monoglycerides) --> cytoplasmic digestion of tri and dipeptides (so when they are dumped into the blood they are individual aas just like the monoglycerides); endopeptidases hydrolyze interior peptide bonds of proteins; exopeptidases hydrolyze terminal AAs; aminopeptidase (an enzyme in the brush border of the small intestine) will cleave a single aa from the aminoterminal; carboxypeptidase (a digestive enzyme present in pancreatic juice) will cleave a single aa from the carboylic end of the peptide

activation of luminal proteases

in the stomach need pepsinogen-->pepsin (10-15% of protein digestion); in the small intestine need trypsinogen-->trypsin with the help of brush border enterokinase; trypsin then activates other enzyzmes (aka pancreatic zymogens or proenzymes); this makes sure that the enzymes don't autodigest the pancreas; absence of trypsin alone makes it appear as if all of the pancreatic enzymes are missing; enterokinase is also called enteropeptidase; all but enterokinase are luminal enzymes; trypsin can break down trypsinogen into trypsin; carboxypeptidases and aminopeptidases are exopeptidases

the breakdown of dipeptides into amino acids

happens inside the cells of the mucosa

the 2 major pancreatic proteases are

trypsin and chymotrypsin; they cannot digest proteins and peptides to single amino acids

trypsin inhibitor

secretory vesicles contain this to serve as a safeguard should pancreatic trypsinogen be activated to trypsin; following exocytosis this inhibitor is diluted out and becomes ineffective

enteropeptidase (enterokinase) deficiency

enterokinase is an intestinal mucosal (membrane) enzyme; responsible for initiating the activation of pancreatic proteolytic proenzymes; catalyzes conversion of trypsinogen to trypsin; its absence present in neonatal period with diarrhea, failure to thrive, edema, and hypoproteinemia; diagnosis is confirmed when trypsin activity in duodenal fluid is low or absent; activity returns after addition of enterokinase; lipase and amylase activity levels are within reference ranges (no pancreatic injury)

acute pancreatitis

pancreatitis is the inflammation and autodigestion of the pancreas; in acute pancreatitis, digestive enzymes and lysosomal hydrolases are co localized; this co-localization mechanism results in activation of the digestive enzymes (esp. trypsin); activated pancreatic enzymes are then released from acinar cells

digestion, absorption, and transport of oligopeptides and aas

on luminal (apical) surface AA peptidases and transporters form an assembly line to digest peptides; peptides absorbed as free aas and di and tripeptides; absorption of aas is absolutely dependent on the electrochemical gradient of Na+ across the epithelium; 4 different Na+ dependent AA transporters; luminal Na+ aa transporters can be electrogenic, secondary active transport; APICAL H+/oligopeptide transporter (PepT1) (ALSO TRANSPORTS DIPEPTIDE-LIKE ANTIBIOTICS); most peptides exit basolateral membrane as aas; basolateral transport is not dependent on Na+ gradients

4 forms of AAs

polar, nonpolar, charged, and uncharged

aas are absorbed by

Na+ co-transporters

di and tripeptidases are absorbed by

H+ cotransporters

PepT1

is a member of the solute-carrier (SLC) super family; because of the vital role that PEPT1 plays in normal homeostasis mutations that result in loss of activity likely have a high negative evolutionary selection pressure

kinetic advantage of oligopeptide absorption

tripeptide/dipeptide uptake more rapid than AA uptake due to higher effectiveness of oligopeptide transporter (PEPT1)

HARTNUP DISEASE

a metabolic disorder affecting absorption of nonpolar aas (particularly tryptophan that can be, in turn, converted into serotonin, melatonin, and niacin); most common metabolic condition involving aas; manifests during infancy or early childhood; they cannot absorb some things (like phanylalanine) as a peptide but can if it is made into a dipeptide (combined with another aa)

protein absorption summary- percentages of absorption

50% of digested protein comes from diet, 25% from protein in the digestive juices, and 25% from desquamated mucosal cells

protein absorption- peptides are absorbed as

aas and dipeptides/tripeptides

protein absorption- absorption of aas/dipeptides/tripeptides is what kind of transport

secondary active transport that may be electrogenic

protein absorption summary- kinetic advantage=

dipeptides/tripeptides are absorbed more efficiently than aas

protein absorption summary- rapid absorption takes place in

the duodenum and jejeunum, much less so in the ileum

protein absorption- protein reaching the colon is metabolized by

bacteria

recommended lipid digestion

70 g/day (30% of caloric intake)

dietary composition of lipids

triacylglycerols (TAGS) 90%; phospholipids 5%; cholesterol 0.5%; fat soluble vitamins and lipid soluble toxins and carcinogens form the remainder

what is the major satiety signal

fat

steps in lipid digestion

emulsification (a mix of 2 immiscible (unblendable) liquids; many are oil/water emultions; this increases the surface area avaible for digestion manu 1000 fold) --> mucelle formation --> enzymatic hydrolysis

the process of emulsification

combined mechanical and enzymatic process; as emulsification progresses surface area for water soluble enzymes increases; in stomach antral peristalsis and slow gastric emptying aid in formation of emulsion droplets and pre-duodenal lipases (lingual and gastric (the 2 acidic lipases that do not require bile acid or co-lipase for optimal enzymatic activity) are active in healthy humans (e.g. 15% of fat digestion occurs in stomach); gastric lipase is an acidic lipase secreted by the gastric chief cells in the fundic mucosa int he stomach; in duodenum pancreatic lipid digestion products (emulsifiers) and bile salts produce micelles;

conversion of emulsion droplet to micelle

pancreatic lipase hydrolyzes surface TEGs drawing TAGs from core causing the emulsion droplet to shrink; budding of multilamellar vesicles; addition of more bile salts produces unilamellar vesicles; further addition of bile salts leads to formation of mixed micelle with hydrophobic lipid tails facing inward and polar head groups facing outward; it is the monoglycerides and fatty acids that are free in solution that are absorbed NOT the micelles; some absorption may be facilitated by specific transport proteins (e.g. for cholesterol)

lysophospholipid

any derivative of a phospholipid in which one of both acyl derivatives have been removed by hydrolysis

3 major classes of dietary fat

triglyceride (90%), cholesterol ester (0.5%), phospholipid (5%)

triglycerides are broken down by

lingual, gastric, and pancreatic lipases into monoglycerides and fatty acids

cholesterol esters are broken down by

cholesterol ester hydrolase into cholesterol and fatty acids

phospholipids are broken down by

phospholipase A2 into lysolecithin and fatty acids

in the newborn

lingual and gastric lipase are essential for the digestion of milk fat because they can penetrate into the milk fat globule and initiate the digestive process;

pancreatic (TAG) lipase

water soluble enzyme only active at oil-water interface; secreted in active form; pH optimum 8.0; hydrolyzes TAGs to FAs and 2-MG (2-monoacylglycerol); needs bile salts to work but is also inhibited by bile salts so needs colipase to prevent inhibition

colipase dependent pancreatic lipase activity

pro-colipase is an inactive form secreted by the pancreas and activated in the intestinal lumen by trypsin; colipase is required to aid in binding of pancreatic lipase to the micellar lipid-water interface; bile salts promote micelle formation but inhibit lipase activity; colipase anchors lipase to fat droplet water interface preventing displacement of lipase by bile salts; in other words colipase prevents the inhibitory effect of bile salts on lipase activity; colipase deficiency can present as a pediatric malabsorption syndrome with chronic diarrhea, abdominal distention, and failure to thrive

cholesterol hydrolase

secreted as active enzyme; hydrolyses cholesterol esters to FA and cholesterol; also hydrolyzes TAG ester linkage yielding glycerol; 2 cholesterol ester hydrolases= acid hydrolase with pH optimum of 4.5-5 and neutral hydrolase with pH optimum of 7.5

phospholipase A2

secreted as proenzyme; activated by trypsin; pH optimum 7.5; requires bile salts; hydrolyzes phospholipids to FA and lysophospholipids (any derivative of a phospholipid in which on or both acyl derivatives have been removed by hydrolysis)

the major products of lipid digestion enter what

the enterocyte by simple diffusion across the plasma membrane (diffusion of mixed micelles through unstirred layer is rate limiting step); saturated solution near brush border; fat digestion products may also have specific transports (e.g. Na-FA symporter for long chain FAs, ABC superfamily cholesterol efflux pumps)

chylomicron transport

exogenous lipids to peripheral tissues where triacylglycerides are unloaded by the activity of lipoprotein lipase

the 3 main stages in the chylomicron's life cycle

nascent, mature, and chylomicron remnant; remnant chylomicrons are those returning to the liver

apoE

a protein which halps carry cholexterol and fat

short chain fatty acid (SCFA) transport

across the colon; may occur by nonionic diffusion and/or via apical membrane SCFA/HCO3- exchange; SCFAs are predominantly from bacterial metabolism of CHOs and are absorbed almost exclusively from the colon; SCFAs are a major component of stool water and are responsible for the diarrhea associated with CHO malabsorption

stool fat is from

is not ingested fat but is from colonic bacteria and epithelial cells

summary of lipid breakdown product absorption

micellar transport of lipid breakdown products to the surface of the enterocyte; mixed micelles carry lipids through the acidic unstirred layer to the surface of the enterocyte; 2-MAG, fatty acids, lysophospholipids, and cholesterol leave the mixed micelle and enter an acidic microenvironment created by an apical Na-H exchanger; the acidity favors the protonation of the fatty acids; the lipids enter the enterocyte by- nonionic diffusion, incorporation into the enterocyte membrane (collision), and carrier mediated transport

chylomicrons in mesenteric lymph nodes and serum

when large numbers of chylomicrons are being absorbed the lymph draining from the small intestine appears milky and the lymphatics are easy to see

summary: emulsion droplets begin to form in the

stomach

summary: micelles are formed in

the small intestine through actions of bile salts and pancreatic (TAG) lipase and co-lipase dependent pancreatic lipase activity

summary: monoglycerides and free FAs diffuse from

micelles through the unstirred layer of primarily jejunal mucosa into the enterocyte

summary: specific apical carriers for

FAs, PLs, and cholesterol

summary: chylomicrons are formed from

re esterified lipids and apoproteins in enterocytes

summary: chylomicrons exit via

exocytosis and transport dietary (exogenous) lipids into lacteals, thoracic duct, and finally the bloodstream

summary: medium chain FAs can diffuse

passively across the mucosa into portal blood (suitable fate substitutions in pts with fat malabsorption) (the processes we described above were for long chain fatty acids) (short chains are not found in out diet so we don't worry about them)

the H2 breath test is used to diagnose lactose intolerance. if a lactose intolerant individual drinks a lactose containing beverage: a. plasma glucose rises within an hr and excess H2 in the breath occurs after 1 to 2 hrs b. elevated plasma glucose and excess H2 int he breath occurs after 1 to 2 hrs c. plasma glucose rises minimally within an hr and excess H2 in the breath occurs after 1 to 2 hrs d. elevated plasma glucose and excess H2 in the breath occurs within an hr

plasma glucose rises minimally (can't breath down lactose into glucose) within an hr and excess H2 in the breath occurs after 1 to 2 hrs

enterokinase deficiency results in severe failure to thrive in affected infants. diagnosis is confirmed by: a. trypsin activity in colonic fluid is low or absent and activity returns after the addition of enterokinase b. trypsin activity in colonic fluid is low or absent an activity returns after the addition of enterokinase c. enterokinase activity in duodenal fluid is low or absent and activity returns after the addition of trypsin d. trysin activity is duodenal fluid is low or absent and activity returns after the addition of enterokinase e. trypsinogen activity in duodenal fluid is slow or absent and activity returns after the addition of enterokinase

trypsin activity in duodenal fluid is low or absent and activity returns after the addition of enterokinase

with regards to co-lipase dependent pancreatic lipase activity a. pro-co-lipase is an inactive contact enzyme that is activated in the intestine by trypsin b. pro-co-lipase is secreted from the intestinal mucosa an inactive form and activated in the intestine by trypsin c. pro-co-lipase is secreted from the pancreas in an inactive form and activated in the intestine by trypsin d. co-lipase is secreted from the pancreas in an inactive form and activated in the intestine by trypsin

pro-co-lipase is secreted form the pancreas in an inactive form and activated in the intestine by trypsin