9/30 Carbohydrate and Protein Digestion/Absorption Flashcards
accessory organs
salivary glands
liver
gall bladder
pancreas
role of salivary glands
in the mouth, moisten food, produce salivary amylase to begin digestion of carbs and salivary lipase to begin digestion of fats
role of liver
creates bile for fat digestion, detoxes blood, processed absorbed vitamins
role of gall bladder
stores bile produced by the liver, releases into duodenum
role of pancreas
secreates pancreatic juices into the duodenum
enzymes produced by stomach
Parietal cells secrete HCl and Intrinsic Factor
Gastric lipase (fat digestion)
pepsin (protein digestion)
pancreas secretions
pancreatic amylase (carb digestion)
pancreatic lipase (fat digestion)
trypsinogen (protein digestion)
chymotrypsinogen (protein digestion)
procarboxypeptidase (protein digestion)
proelastase (protein digestion)
bicarbonate (to neutralize acid)
role of small intestines
digestion and absorption of macromolecules
role of large intestines
water reuptake, bacteria produce vitamins/LI absorbs them
components of maltose/isomaltose
glucose disaccharide
components of sucrose
disaccharide of glucose and fructose
components of lactose
disachharide of glucose and galactose
three major dietary carbohydrates
starch, sucrose, and fructose
role of salivary amylase
begins breakdown of starches and complex carbs into oligosaccharides, tri’s and di’s
role of pancreatic amylase
further breakdown of starches and complex carbs into oligosaccharides, tri’s and di’s in the lumen of the small intestines
enzymes produced by small intestines
(iso)maltase
sucrase
lactase
role of (iso)maltase
breaks starch oli’s/tri’s/di’s into monosaccharide glucose in brush border
role of sucrase
breaks down sucrose disaccharides into glucose and fructose monosaccharides in brush border
role of lactase
breaks down lactose disaccharides into glucose and galactose monosaccharides in brush border
things that can affect salivary gland function
radiation therapy, chemotherapy, and HIV
indigestible carbs
B-linkages of cellulose
Raffinose in beans
mechanism of carb uptake into enterocytes
Secondary active transport, uses the gradient of Na+ to drive uptake of glucose and galactose, SGLT1 ([Na+] higher outside cell)
Facilitated transport, fructose is transported into cell by GLUT5 transporter
mechanism of monosaccharides from enterocytes to blood
facilitated transport
glucose/galactose/fructose: GLUT2
Essential Amino Acids
“private tim hall” “pvt tim hall”
phenylalanine
valine
threonine
tryptophan
isoleucine
methionine
histidine
(arginine for growth in babies)
leucine
lysine
zymogen
inactive protein precursor for proteases, also called proenzymes, start with pro- or end with -gen
must be trimmed by a protease or peptidase, modifications are irreversible
pepsinogen
zymogen of pepsin
under acidic conditions, structure changes and autocleavage to pepsin, an active protease
trypsinogen activation
enteropeptidase activates (made in intestinal cells)
function of trypsin
digests protein and activates other pancreatic zymogens (chymotrypsinogen, proelastase, procarboxypeptidase)
daily protein recommendations
0.8g/kg body weight
50g women
60g men
consequences of protein malnutrition
growth retardation
increased learning failure
chronic illness later in life
lactose intolerance
failure to digest/absorp lactose so the bacterial in the gut metabolize it instead
CF: diarrhea, steatorrhea, abdom discomfort, distention, flatulence
kwashiorkor
protein deficiency but not hypocaloric
more common in developing countries, associated with war and famine
CF: muscle wasting, decrease of plasma proteins (causes osmotic imblance that causes GI imbalance, swelling of gut, edema, and water retention)
marasmus
hypocaloric but no missing nutrients
CF: muscle wasting but NO edema
amino acid absorption
interstitial lumen to enterocyte (secondary active transport)
enterocyte to hepatic portal vein (facilitated transport)
hartnup disease
neutral amino aciduria
rare AR disorder of Na+ dependant transporter, intestinal and kidney epithelial cells can’t absorb neutral or aromatic AAs
kidneys: increase in AA in urine (hyperaminoaciduria)
intestines: malabsorption –> deficiency of essential AAs
CF: (Pellagra-like) 3Ds (diarrhea, dementia (w/ hallucinations), and dermatitis (photosensitive rash), ataxia
Pellagra from deficience in tryptophan or niacin, can lead to decrease in NAD/NADP, women more affected because estrogen inhibits tryptophan degredation to niacin
Treatment: oral niacin (but hyperaminoaciduria remains)
cystinuria
rare AR disorder involving transporter proteins (SLC3A1 and SLC7A9)
kidneys or intestines can’t resorb cystine and basic amino acids (COLA, cystine, ornithine, lysine, arginin)
CF: insolubility of cystine generates kidney stones that block ureter, hematuria, severe pain (renal colic), and hyperaminoaciduria
