DLA 16 and Lecture 27+28

Question 1

digestion in the mouth

Answer 1

carbohydrate digestion by salivary alpha amylase

this enzyme cleaves alpha 1,4 bonds of starch and glycogen and forms branched oligosaccharides

lingual lipase for lipid digestion
released in the mouth but mainly swallowed

Question 2

digestion in the stomach

Answer 2

gastrin

leads to HCl release from parietal cells
release of pepsinogen and gastric lipase from chief cells.

Question 3

role of HCl in the stomach

Answer 3

HCl denatures food; leads to quicker digestion

destroys fungi and bacteria

alters the conformation of pepsinogen to pepsin; autocatalytic activation

pepsin cleaves peptide bonds within the protein (endopeptidase)

Question 4

acidic chyme in the stomach

Answer 4

stops carb digestion… salivary amylase is denatured

protein digestion starts from pepsin

breakdown of TAGs

Question 5

role of secretin and CCK

Answer 5

when the acidic chyme reaches the duodenum, these enzymes are released to assist with neutralizing the pH

Question 6

role of CCK and digestion

Answer 6

release of bile from gallbladder
activation of enteropeptidase enzyme
secretion of pancreatic enzymes

inhibition of gastric motility; allows pH change

Question 7

role of enteropeptidase

Answer 7

activates zymogens:

trypsinogen to trypsin
chymotrypsinogen to chymotrypsin
proelastase to elastase
procarboxypeptidases to carboxypeptidases

for lipids:
prophospholipase A2 to phospholipase A2
procolipase to colipase

Question 8

lactose intolerance

Answer 8

pain, nausea, flatulence, and diarrhea after the consumption of lactose

suppose to be broken down by lactase

Question 9

lactase synthesis

Answer 9

The LCT gene for lactase is generally less expressed after infancy (lactase non-persistence phenotype)

The gene expression is controlled by MCM6

inherited changes to this leads to prolonged synthesis of lactase (lactase persistence phenotype)

Question 10

abnormal lactose metabolism

Answer 10

lactase deficiency will lead to lactose reaching the large intestine.

the gut bacteria degrade the lactose to osmotically active compounds and thus lead to symptoms

osmotic diarrhea- water entering the lumen from cells

Question 11

treatment of lactose intolerance

Answer 11

diet low in lactose
lactose free products
lactase pill

Question 12

forms of lactose intolerance

Answer 12

1. lactase non-persistence or primary lactose intolerance

lactase is strongly reduced after age 7
adult hypolactasia

2. disaccharide deficiency - secondary lactose intolerance

all disaccharides are affected, but lactase is the first activity lost
can occur due to food poisoning
rotavirus
celiac disease

3. congenital lactase deficiency (most severe and most rare form )

symptoms as a baby
need lactose free formula

Question 13

activation of trypsin

Answer 13

trypsinogen is released into the duodenum by the pancreas

activated when it reaches the lumen; due to it being a powerful enzyme

activated by enteropeptidase

Question 14

once trypsin is activated what does this enzyme activate

Answer 14

chymotrypsin
elastase
carboxypeptidase

phospholipase A
colipase

Question 15

where does trypsin cleave

Answer 15

after arginine or lysine

Question 16

where does chymotrypsin cleave

Answer 16

after bulky and aromatic residues

Question 17

where does elastase cleave

Answer 17

glycine, alanine, and serine

Question 18

where does carboxypeptidase cleave

Answer 18

cleave from the carboxy-end

Question 19

absorption of AA’s

Answer 19

done mainly by secondary active transport with the co-transport with Na

the release of AA’s into the portal vein is by facilitated diffusion

Question 20

absorption of monosaccharides

Answer 20

dietary fructose enters the intestinal cell via facilitated transport via GLUT 5

dietary glucose and galactose will enter the intestinal cell via SGLT-1
secondary active transport with Na

all three monosaccharides are released via facilitated transport by GLUT-2 into the portal vein

Question 21

function of bile salts?

Answer 21

1. transportation of free cholesterol and conjugated bilirubin from the liver to duodenum
2. emulsify dietary lipids for digestion
3. form mixed micelles for the uptake of lipids into the mucosal cells

Question 22

colipase action?

Answer 22

The protein colipase pushes bile salts away from TAGs and anchors pancreatic lipase to the lipid droplet.

Question 23

pancreatic lipase function

Answer 23

cleaves TAGs only to MAG’s

Question 24

Orlistat

Answer 24

a drug used to inhibit pancreatic lipase for weight loss treatment

Question 25

end product of nucleic acids

Answer 25

uric acid that is released into the urine

Question 26

possible causes of steatorrhea

Answer 26

1. lack of conjugated bile salts due to liver damage, bile duct obstruction, and/or pancreatic tumor 2. defects related to pancreatic secretions deficiency in enzymes 3. defective intestinal cells or shortened bowl

Question 27

what reactions require BH4 as a cofactor

Answer 27

phenylalanine hydroxylase (Phe to Tyr) tyrosine hydroxylase (Tyr to DOPA) tryptophan hydroxylase (Trp to 5-hydroxy tryptophan)

Question 28

PKU II or malignant PKU

Answer 28

deficiency of BH2 or dihydrobiopterin reductase much more severe CNS symptoms: decreased neurotransmitter synthesis (serotonin, dopamine, Epi, and Norepi) treatment includes Phe diet restriction and providing dietary biopterin treatment can also be saproterin or an analogue of BH4

Question 29

biochemical defect of PKU II

Answer 29

No BH2 and/or no dihydrobiopterin reductase deceased melanin synthesis and decreased neurotransmitter synthesis tyrosine becomes essential AA increase in phenylpyruvic acid

Question 30

Tetrahydrobiopterin deficiency

Answer 30

results in hyperphenylalaninemia and decrease synthesis of neurotransmitters results in intellectual disability and seizures management: provisional neurotransmitters dietary restriction of phe

Question 31

S-adenosyl methionine (SAM)

Answer 31

synthesized from methionine A methyl group donor in many reactions after the donation of the methyl group SAM is converted to homocysteine homocysteine may be converted to cysteine by transsulfuation pathway (need PLP or B6) or conversion back to methionine by B12 and methylfolate

Question 32

importance of 1-carbon pool

Answer 32

products formed are purines and pyrimidines required for DNA and RNA synthesis (cell division)

Question 33

folate deficiency

Answer 33

reduction in 1-C donors, thus reduced synthesis of purines and pyrimidines delay in DNA synthesis, thus reduced rates of cell division effects on RBC formation- see macrocytes and megaloblasts decrease in hemoglobin concentration polysegmented neutrophils

Question 34

who is at risk for folate deficiency?

Answer 34

those who are pregnant (neural tube defects) chronic alcohol consumption those who do not eat vegetables (green, leafy)

Question 35

histamine load test????

Answer 35

used to determine folate deficiency in folate deficiency, it is seen that histamine metabolism is limited and FIGLU accumulates more FIGLU in the urine

Question 36

Vitamin B12 deficiency

Answer 36

macrocytic anemia and neurological features (tingling in hands/feet, inability to walk, psychiatric, and urinary incontinence) usually absorbed in the terminal ileum with intrinsic factor (released by parietal cells) have increased levels of methylmalonate in circulation and in urine elevated homocysteine levels have normal levels of un-usable folate (methyl THF form)

Question 37

functions of B12

Answer 37

animal sources are rich in vitamin B12 needed for methionine synthase needed for methylmalonyl CoA mutase

Question 38

reactions that need B12?

Answer 38

conversion of homocysteine into methionine via methionine synthase conversion of methylmalonyl CoA to succinyl CoA via methylmalonyl CoA mutase

Question 39

folate trap

Answer 39

when one does not have correct levels of vitamin B12 the cellular folate is stuck in the methyl-THF form cannot be converted back bc the reaction is not reversible

Question 40

who is at risk for B12 deficiency

Answer 40

Vit. B12 is stored in the liver, so it takes some time to develop a lack of B12 usually seen in vegans or failure to absorb B12 due to atrophic gastritis pernicious anemia disease of the ileum

Question 41

diff between folate and B12 deficiency

Answer 41

In vitamin B12 deficiency one will see neurological manifestations and an increase in methylmalonate