Nutrient Digestion and Absorption

luminal hydrolysis

pancreatic enzymes, digested in the lumen

Brush border enzymes

finish up the digestion, break em into smaller units

lipids are different in how they get absorbed how

digested then resynthesized

carbs, proteins and lipids are absorbed where

first two feet. dj ile

carbs that escape small intestine are metabolized by

colonic bacteria into short chain fatty acids

calcium, iron, and folate absorbed where

very first part of the duodenum

calcium also in later small intestine

bile acids absorption where

ILEUM also jejunum and ascending colon

cobalamin absoprtion where

beginning of ileum

organ site of celiac disease

blunted villi in duodenum and jejunum

defective fat absorption and lactose hydrolysis

site of chronic pancreatitis

exocrine pancreatitis

site of crohn disease

ileum

defective cobalamin and bila acid resorption

primary lactase deficiency site

small intestine

digestion of starch starts in where with what

in mouth with salivary amylase, not really in stomach

amylase cannot break what linkages

terminal alpha 4 or 1-6 linkage or alpha 1-4 linkage adjacent to branching a1-6 linkage

what can digest terminal alpha 1-4 linkages

glucoamylase

SGLT1

cotransporter, brings in 2 na with sugar/monomer

fuctose goes through which cotransporter

GLUT5

Galactose and glucose can go through whcih transporter

SGT1

what is the exit path for glucose, galactose, adn fructose

GLUT2

lactase deficient individuals hydrolyse less lactose so

less glucose in plasma

colonic bacteria metabolize lactose entering colon which leads to

higher h2 excretion

PepT1 is what

oligopeptide transporter, efficient and increases plasma AA concentration

contransport with H+

what transport maximizes absorption

dipeptide

individual AA transporters are more saturatable

mutation in SLC6A19

hartnup disease

defective proper resorption of neutral AA like phenylalanine, tryptphan (so decreased serotonin, melatonin, niacin)

hartnup disease

failure to thrive, pellagra, photosensitivity, cerebellar atazxia, psych abnormalities

hartnup disease

tx hartnup disease

high protein diet, niacin supplements

mutations in SLC3A1 and SLC7A9

cystinuria

prevents proper reabsoroption of basic or + charged AA (cystine, ornithine, lysine, argininge)

cystinuria

tx cystinuria

hydration, alkalinization of urine

most fat absorbed in __________, rest in ____

first few feet of jejunum

ileum

micelle breakdown products are absorbed by the

enterocyte

colipase importance

without colipase, lipases can’t digest lipid

it anchors lipase to the lipid

in presence of bile salts lipase has trouble doing its job

acid microenvironment near enterocyte

nah antiporter

TAG is digested to ___ by lipases

MAG

MAG gets

absorbed and then resterified to TAG

FFA can also be absorbed and reesterified to TAG

how does TAG leave the enterocyte?

TAG gets incorporated into chylomicrons

travels through lacteals

SC and MC FA how do they enter blood

directly reabsorbed

MAG and LCFA to travel

intochylomicrons and enter lymphatic system

SCFA has how many carbons

<6

MCFA has how many carbon

6-12

LCFA has how many carbons

13-21

VLCFA has how many carbon atoms

>21

pernicious anemia

lack of b12 bc lack of intrinsic factor

what makes IF

parietal cells

where does B12 bind IF

intestine, not stomach

where is B12 absorbed

ileum

how are minerals absorbed

specific channels, transporters or solvent drag or paracellular flux

calcium is reabsorbed where by what channels

duodenum by TRPV6 channels (stim by vit d)

after passing TRPV6, ca binds

calbindin

after binding calbindin, it is transported outside of the cell →

in exchange for hydrogen

regulated pathway of Ca2+ reabsorption

all three steps require vitamin d

enter trpv6 channel

bind calbindin

exhcnage for hydrogen

iron is abosrbed in

duodenum

___ cotransports iron with ___

DMT

H+

Fe2+ is transported in blood on

transferrin

Fe3+ (ferric) is not soluble when

ph>3

hephaestin

oxidizes Fe2+ → Fe3+

what reduces nonheme Fe3+ → Fe2+

dcytb

once inside enterocyte, Fe2+ transfers to

mobilferrin

Fe2+ leaves cell via

ferroportin (FP1)

after hephaestin oxidizes it to Fe3+ (interstitial space)

binds to transferrin in plasma