Amplification of GI Mucosal Surface area
Circular folds: increase surface area 3x
Villi on folds: increases by 30x
On cells of villi: microvilli: 600x increase: largest increase!
Polysaccharides
Starch: from plants, complex
most abundant carb in diet
Glycogen: from animals (meat)
muscle glycogen
Cellulose: Plant cell walls
NOT digestible
Serves as fibers (bulk in GI to aid in motility)
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Amplification of GI Mucosal Surface area
Circular folds: increase surface area 3x
Villi on folds: increases by 30x
On cells of villi: microvilli: 600x increase: largest increase!
Polysaccharides
Starch: from plants, complex
most abundant carb in diet
Glycogen: from animals (meat)
muscle glycogen
Cellulose: Plant cell walls
NOT digestible
Serves as fibers (bulk in GI to aid in motility)
sucrose
table sugar: glucose + fructose (fruit sugar)
Lactose
milk sugar: glucose + galactose
Maltose
glucose + glucose
Disacchardies
Simple sugars:
sucrose
Maltose
maltose
Monosaccharides
Glucose (most abundant)
Fructose
Galactose
Digestion of Carbs
Mouth
Salivary amylase
Initiates digestion (small amt)
Stomach: NONE
Pepsin inactivates amylase
Small intestine
Pancreatic amylase
Majority of carb digestion
Epithelial Disaccharides: In cell membranes
break down disaccharides
Absorption of Carbs
secondary active transport using sodium gradient
From lumen, carrier mediates transport across membrane
Types of lipids
Triglycerides (90%)
2-monoglyceride + fatty acids
Cholesterol
Phosphipids
Digestion of Lipids
Mouth: Lingual lipase
Small Intestine: fat is emulsfied, increasing SA for lipases to break down fats
Pancreatic Lipase
Breaks fats into monoglycerides that are able to cross membrane
Resynthesized into chylomicrons and removed via exocytosis
Low density: high fat, low protein
Tryglyceride core with phospholipid membrane
Picked up by lymphatics
Absorption of fats
Fats and cholesterol are packaged into chylomicrons and released via exocytosis into villia
Lacteals: lymphatic capillary that are highly permeable
Enter circulation via lymphatic system
Proteins Types
proteins
Peptides
Amino acid
Digestion of Proteins
Stomach: pepsin
Small intestine:
pancreatic enzymes
Trypsinogen:
Endopeptidases
Exopeptidases
Epithelial enzymes: in wall of duodenum
Cleaves small peptides (dipeptides, tripeptides) into amino acids
Pancreatic Enzymes: Trypsinogen
activated by enteropeptidase to trypsin, which activates other proeznymes (digestion of proteins)
Pancreatic enzyme: Endopeptidase (3)
cleave internal peptide bones: trypsin, chymotrypsin, elastase
Pancreatic enzyme: Exopeptidases:
cleave terminal peptide bonds: procarboxypeptidases A + B
Absorption of Proteins
has to be broken down into amino acids, if absorbed: immune rxn
take up via secondary active transport and sodium gradient
Di and tripeptides:
more efficiently absorbed than amino acids
Vitamin absorption: fat soluble
A, D, E, K
passively absorbed in small intestine
Can cross membrane
Not well regulated: can lead to toxicity
Water soluble vitamin absorption
Passive and active processes in small intestine
Requires transport mechanisms
vitamin B12 absooprtion and consequence of deficiency
Via intrinsic factor (parietal cells in stomach)
binds with ingested B12
Receptor-mediated endocytosis in small intestine of B12 intrisinc factor complex that releases into blood
Consequence
Shiny red tongue
Pernicious anemia: inability to form RBCs, lack of O2, fatigued
B12 is needed for
RBC synthesis
Calcium absorption
does not cross membrane
high conc in gut
moves down concentration gradient thru calcium channels
CaBP: calcium binding protein
Transported out/in by primary active transport thru ATPase
Vitamin D increases CaBP and Ca ATPase
steroid that changes gene expression, takes a few hours
Why is iron absoprtion ususal?
Toxic molecule: oxidizes membranes and produces problems
Keep it bound to protein: heme
Iron Absorption
iron and heme absorbed by DMT-1: facilitated diffusion
heme iron absorbed by heme transporter
Equilibrates with ferritin (holds thousands of Iron molecules)
In gut epithelial cells: storage of iron
Elimination of iron
keeping iron in ferritin is a way of eliminating:
lost with enterocytes (they turnover rapidly and ferritin is removed with them)
Eliminated in feces
Free iron is transported out into circulation where it beings with transferrin in plasma
low plasma iron/iron deficiency
increase DMT-1: take up more iron from gut lumen
Increase ferraportin: more transfer into plasma
Decrease ferritin: decrease storage/elimination (more goes into plasma)
iron excess
decrease DMT-1: less iron take up from gut lumen
Decrease ferraportin:
from liver produced hepcidin
Increase ferritin: iron is trapped in ferritin and lost as enterocytes are sloughed off from gut lining