Biochem 46

Front 1

fenestrations in sinus endothelium cells of liver

Back 1

mean diameter 100 nm-free diffusion of small molecules, but not particles the size of chylomicrons (chylomicron remnants are smaller and can pass directly to hepatocytes)

Front 2

1/4 of liver lysosomes are located

Back 2

in Kupffer cells

Front 3

stellate cells (aka perisinusoidal or Ito cells) fxns

Back 3

lipis filled cells and serve as primary storage site for vit A; control hepatic CT turnover and ECM, regulate contractility of sinusoids

Front 4

pit cells

Back 4

NK cells; liver-associated lymphocytes

Front 5

xenobiotics

Back 5

cmpds with no nutritional value and are potentially toxic

Front 6

phase 1 rxn

Back 6

take lipophilic cmpd and oxidize, hydroxylate, or hydrolyze via enzymes

Front 7

conjugation aka phase II rxns

Back 7

add negatively charged group like glycine or sulfate to molecule

Front 8

what is used to clear steroid hormones from circulation

Back 8

sulfation

Front 9

what can sulfate be obtained from

Back 9

degradation of cysteine or methionine

Front 10

P450-dependent mono-oxygenase system

Back 10

oxidative, peroxidative, reductive degradation of exogenous or endogenous substances

Front 11

key enzymatic components of P450 system

Back 11

flavoprotein NADPH-cytochrome P450 oxidoreductase and cytochrome P450

Front 12

cytochrome P450 fxn

Back 12

terminal e- acceptor and substrate-binding site of microsomal mixed-function oxidase complex

Front 13

nomenclature of P450 enzymes

Back 13

CYP2E1 = CYP is cytochrome P450 family, 2 is subfamily, and E denotes ethanol, and 1 denotes specific isoenzyme

Front 14

CYP3A4

Back 14

accounts for 60% CYP450 enzymes in liver and 70% cytochrome enzymes in gut wall enterocytes

Front 15

HMGCoA reductase inhibitors require what for degradation

Back 15

CYP3A4

Front 16

cytochrome P450 isoenzyme commonalities

Back 16

found in smooth ER, bound to lipid portion of membrane (phosphatidylcholine), inducible by presense of own best substrate, generate reactive free radical cmpd as intermediate

Front 17

vinyl chloride

Back 17

used in synthesis of plastics and can cause angiosarcoma of liver of exposed workers

Front 18

what is vinyl chloride activated by

Back 18

phase I rxn to reactive epoxide via CYP2E1-product can react with DNA or other cellular molecules

Front 19

Aflatoxin B1

Back 19

made more toxic by P450 (CYP2A1); produced by fungus Aspergillus flavus on peanuts

Front 20

acetaminophen metabolism in liver

Back 20

glucuronylated or sulfated for safe excretion by kidney; toxic intermediate N-acetyl-p-benzoquinoneimine (NAPQI)

Front 21

NAPQI normal formation with acetaminophen therapeutic levels

Back 21

<10% forms NAPQI which can be handled by glutathione detoxifying system (phase II rxn)

Front 22

what enzyme produces NAPQI

Back 22

CYP2E1 (induced by alcohol)

Front 23

how do ammonia groups travel to liver

Back 23

on glutamine and alanine-liver converts teses ammonia nitrogens to urea for excretion in urine

Front 24

what is the only organ that can produce ketone bodies

Back 24

liver, but it can't use them for energy

Front 25

when are ketone bodies produced

Back 25

rate of glucose synthesis is limited and fatty acid oxidation occuring rapidly

Front 26

what does albumin carry

Back 26

fatty acids, steroids, hydrophobic aas, vitamins, drugs

Front 27

portal hypertension causing ruptured esophageal varacies causes

Back 27

bleeding-metabolized by GI bacteria which release ammonium ion and enters portal vein-liver can't handle all the ions and they pass into circulation contributing to hepatic encephalopathy; also, clotting is decreased due to low liver fxn causing prolonged bleeding of varacies

Front 28

O-linked sugars secreted by liver

Back 28

most sugars secreted by liver are O-linked; carb attached to protein at its anomeric carbon through a glycosidic link to -OH of a serine or threonine residue

Front 29

N-linked sugars

Back 29

N-glycosyl link to amide nitrogen of asparagine residue

Front 30

N-acetylneuraminic acid (NANA)

Back 30

aka sialic acid; an O-linked sugar; 9-carbon sugar synthesized from fructose 6-phosphate and phosphoenolpyruvate

Front 31

major fxn of pentose phosphate pathway

Back 31

generation of NADPH and 5-carbon sugars-used to keep glutathione reductase going and generation of ribose

Front 32

what does the liver use NADPH for

Back 32

biosynthesis of fatty acids and cholesterol; also for other biosynthetic rxns like proline synthesis and P450 rxns

Front 33

energy supply for liver

Back 33

ATP, UTP, GTP, reduced NADPH, acyl CoA thioesters

Front 34

major fuels used by liver after mixed meal containing carbs

Back 34

glucose, galactose, and fructose

Front 35

why is glycolysis rate increased after glucose meal

Back 35

PFK-2 active, thus PFK-1 is activated by fructose 2, 6-bisphophate

Front 36

what determines rate liver uses glucose

Back 36

activity level of glucokinase

Front 37

fructose 6-phosphate and glucokinase

Back 37

high levels of fructose 6-phosphate promote interaction of glucokinase with RP

Front 38

high levels of glucose and fructose 1-phosphate with glucokinase

Back 38

block glucokinase from binding RP and promote dissociation

Front 39

when do fructose 2,6-bisphosphate levels increase

Back 39

in presence of insulin-increases glycolysis rate

Front 40

increased glucagon levels cause

Back 40

protein kinase A activation so that PFK-2 is phosphorylated and inactive = glycolysis slows down and gluconeogenesis enhanced

Front 41

major fuel in liver during fasting

Back 41

long-chain fatty acids (palmitic, stearic, and oleic)

Front 42

length of long-chain, medium chain, and short chain fatty acids

Back 42

12-20; 4-12; and 2-4

Front 43

where are sites for oxidation of medium chain fatty acids

Back 43

liver and kidney

Front 44

Zellweger (cerebrohepatorenal) syndrome

Back 44

rare inherited absence of peroxisomes in all tissues; accumulate C26-38 poluenoic acids in brain tissue due to defective peroxismal oxidation for myelin synthesis

Front 45

Peroxisome proliferator-activated receptors (PPARs)

Back 45

role in liver metabolism-in liver, direct activity of genes involved in fatty acid uptake and B and w-oxidation of fatty acids

Front 46

lack of PPARa in mice causes

Back 46

inability to increase rate of fatty acid oxidation leading to excessive fatty acid build up in hepatocytes, inability to make sufficient glucose and ketone bodies

Front 47

major urinary metabolite of aspirin in humans

Back 47

salicylurate

Front 48

why is there a relatively high level of triacylglycerols in ppl w/acute and chronic hepatitis, cirrhosis, or other diffuse hepatocellular disorders

Back 48

activities of both LPL (lipoprotein lipase) and HTGL (hepatic triglyceride lipase) are reduced

Front 49

Low LCAT levels with high triavylglycerol levels cause what composition changes in LDL particles

Back 49

high triacylglycerol and cholesterol ester poor

Front 50

branch-chain aas that can be used as fuel by most cell types

Back 50

valine, leucine, and isoleucine

Front 51

how do skeletal muscles, kidney, and intestinal mucosa send nitrogen to liver

Back 51

alanine

Front 52

how do skeletal muscles, lungs, and neural tissues send nitrogen to liver

Back 52

glutamine

Front 53

what other way does the kidney send nitrogen to liver

Back 53

serine