Cell Bio 3 Flashcards

Question

glycogen storage dz vs therapy

Answer 1

inability to make/break glycogen nmlly --> pt's liver can't produce glu to release in blood --> hypoglycemia or muscle cramps d/t low energy vs small freq snacks to maintain glu (for liver); reduce exer or muscle fatigue to prevent cramps or supplement w/ higher dietary glu and aa (for muscle)

Answer 2

key metabolite: help with FA synthesis, chol synthesis, neurotransmitter synthesis, nucleotide synthesis, glutathione defense system against ROS esp in RBC, NADPH oxidase uses NADPH to make superoxide --> help mac kill, drug detox

Answer 3

oxidative phase: net 2 NADPH made, 1st and 3rd steps = inhibited by NADPH/activated by NADP+; G6P = [O] to 6-phosphogluco-delta-lactone via G6P dehydrogenase (rate limiting step) --> 6-phosphogluco-delta-lactone to 6-phosphogluconate --> 6-phosphogluconate = decarboxylated to Ru5P via 6-phosphogluconate dehydrogenase vs non-oxidative phase: Part 1 = 2 isomerizations of Ru5P and Part 2: pentose molec converted to glycolysis/gluconeogenesis intermediates

Answer 4

(glu-α-1,2-fru) vs (gal-β-1,4-glu) vs (glu-α-1,4-glu) vs (glu-α-1,6-glu)

Answer 5

fru = phosphorylated at C1 by fructokinase using 1 ATP --> F1P = cleaved by aldolase B to make DHAP + glyceraldehyde (if defic in aldolase B --> F1P inc --> bad) --> glyceraldehyde = phosphorylated by triose kinase and used 1 ATP --> G3P vs fru = phosphorylated at C6 by hexokinase to make F6P to do glycolysis. aldolase B defic --> high F1P --> bad --> ppl need to avoid fru

Answer 6

glu = reduced to sorbitol --> sorbitol = oxidized at C2 to make fru

Answer 7

gal = phosphorylated at C1 by galactose kinase using 1 ATP to make gal1P --> gal1P reacts w/ UDP-glu to make G1P and UDP-galactose --> UDP galactose = converted to UDP-glu by epimerase

Answer 8

can't form UDP-gal or make molec dependent on UDP-gal --> gal1P inc in liver --> bad vs galactokinase = deficient or can't be processed

Answer 9

UDP-gal and UDP-glu help w/ synthesis of glycoproteins, glycolipids & proteoglycans; UDP =-gal also help form lactose in mammary gland

Answer 10

UDP-glu = oxidized to UDP-glucuronate --> has stable b/c of neg charge --> help inc solubility of molec it's attached to; ex: bilirubin = insoluble but becomes soluble by adding 2 glucuronides. glucuronate can be modified to final form like GAGs or amino sugars

Answer 11

glu from food enters blood via gut vs liver uses glycogen/precursor to make glu and send out to blood vs liver uses precursor (glycerol from adipose to FA, lactate from anaerobic glycolysis in muscle or RBC, aa from protein degrad in skel muscle esp ala) to make glu and send out to blood => gluconeogenesis

Answer 12

lactate to pyru via lactate dehydrogenase and NAD+ (becomes NADH when forming pyru) vs ala to pyru via ala transferase. glycerol to DHAP via glycerol kinase

Answer 13

PEP to pyru = irreversible --> can't go pyru to PEP --> pyru to oxalo in mito via pyru carboxylase --> oxalo uses mal/asp shuttle to go to cyto --> oxalo to PEP via PEP carboxykinase + GTP. key point: can bypass irreversible step but requires energy

Answer 14

FBP = dephosphorylated to F6P via FBPhosphatase --> F6P to G6P

Answer 15

high AMP, F2,6P, insulin vs high ATP

Answer 16

G6P = dephosphorylated to glu via G6Phosphatase, rxn = inside ER lumen

Answer 17

liver does glycogenolysis to make glu for body, muscle does glycogenolysis to make glu for itself vs brain and RBC does gluconeo to make glu for blood stream

Answer 18

liver makes glycogen and FAs, adipose takes FA and stores as TAGs; muscle makes glycogen

Answer 19

intake > need --> wt gain intake < need --> wt loss

Answer 20

digest quickly, mono (glu, fru, gal), disacch (su, lac, malt) vs digest slowly, oligo/polysacch (starch, glycogen, dietary fiber). fruits, starch, milk

Answer 21

carb (40-60%)

Answer 22

rapid effects on blood glu lvl vs slower effects on blood glu lvl --> glu doesn't rise fast enough vs more like nondigestible fiber than starch, glu homeostasis -> glu doesn't rise fast enough, reduce postprandial inulin requirement

Answer 23

mouth (salivary alpha amylase breaks alpha1,4 glu bonds) thru stomach (HCl inactivates salivary alpha amylase) to sm intestines (pancreatic alpha amylase produces malt, isomalt, oligosacch)

Answer 24

dec transit time thru sm intestines (ie. moves faster) --> inc fecal bulk, help intestinal flow vs no effect on transit time thru sm intestines --> create gelatinous mold, delay gastric emptying, dec absorption of chol and glu, soft stool d/t H2O absorption

Answer 25

25-38g/d vs 10g/d

Answer 26

slow sugar absorption --> slow rise in blood glu, promote good microbiota, bacteria breaks down complex carbs, uses monosacch for ATP prod, produces short chain FA

Answer 27

value for single food item based on how slowly or quick it causes an inc in blood glu lvls after eating, reference = usually white bread. higher glycemic response --> sugar high --> crash vs lower glycemic response --> less dramatic effect on blood glu

Answer 28

Acetyl CoA can’t diffuse from mito to cyto, but citrate can. Citrate diffuses from mito to cyto —> citrate lyase breaks cit into acetyl CoA (starting material) and oxalo —> oxalo can be converted back to pyruvate and yield NADPH in the process. acetyl CoA carboxylase (irreversible/committed/rate limiting step), ATP, and CO2 converts acetyl CoA to yield malonyl CoA and ADP + Pi —> FA synthase + acyl carrier protein/ACP and 2 NADPH converts malonyl CoA to yield palmitic acid (C16H32O2), water, and CO2 cycle rpts 7x

Answer 29

malic enzyme can supply NADPH

Answer 30

malonyl CoA attaches to -SH of ACP

Answer 31

high insulin dephosphorylates enzyme --> active, high cit vs AMP-activated protein kinase phosphorylates enzyme --> inactive, high palmitoyl CoA

Answer 32

can't introduce 2x bonds after C10, and ONLY do them at C5/6/9. start w/ essential FA linoleic acid --> add 2x bonds as much as we can --> elongase will lengthen chain 2C's at a time via malonyl CoA condensation and reduction --> add more 2x bonds as much as we can; happens in cyto face of ER

Answer 33

stabilizes cell membrane, precursor for bile salts and steroids; can make ubiquinone, dolichol for glycoprotein synthesis, cholecalciferol (active vit D) vs from acetyl CoA in liver/intestine, from animal products like egg/red meats/liver

Answer 34

Acetyl CoA can’t diffuse from mito to cyto, but citrate can. Citrate diffuses from mito to cyto —> citrate lyase breaks cit into acetyl CoA (starting material) and oxalo —> oxalo can be converted back to pyruvate and yield NADPH in the process. 2 acetyl CoAs condense to make acetoacetyl CoA --> 3rd acetyl CoA added => HMG-CoA --> HMG-CoA reductase (committed/rate limiting) + 2 NADPH reduce HMG-CoA to mevalonate --> mevalonate to isopentenyl pyrophosphate to squalene

Answer 35

high insulin --> phosphatase deP HMG-CoA reductase --> active --> HMG-CoA to mevalonate --> chol vs high glucagon --> AMP mediated protein kinase phosphorylates HMG-CoA reductase --> inactive --> no chol; high AMP/low ATP or high sterol --> HMG-CoA reductase = inactive

Answer 36

in ER. high chol --> chol bind to SCAP --> SREBP inactive. low chol --> chol doesn't bind to SCAP --> SREBP active --> S2P cleaves DNA binding domain of SREBP --> DNA transcpxn --> chol synthesis

Answer 37

Acyl:chol acyltransferase (ACAT) --> store chol for steroid synth, in cells. lecithin:chol acyltransferase (LCAT) --> esterifies chol associated w/ HDL, in blood. -OH group at C3 of chol = esterified to be FA --> inc hydrophobicity of chol --> inc solubility in lipoproteins

Answer 38

bile acid/salt = more polar/hydrophilic than chol; emulsify dietary lipids in sm intestines for digestion; cyt P450 monooxygenase + NADPH and 7-alpha-hydroxylase incorporates -OH (committed/rate-limiting). cholecystokinin signals gallbladder to release bile

Answer 39

in liver and sent to gallbladder, has all hydroxy groups (3 for cholic acid, 2 for chenodeoxycholic acid) vs modified by gut bacteria, lack -OH at C7. lithocholic acid = only -OH at C3 --> least soluble --> excreted

Answer 40

aldosterone, cortisol, estrone, estradiol. CHOL = STARTING MATERIAL; tissue dependent synthesis

Answer 41

made in gut --> carry dietary TAG from intestine to peripheral/muscle/adipose tissue; deliver chol and phospholipids to liver; HAS APO B48 vs made in liver --> carry endogenously synthesized TAG, chol, and chol esters from liver to muscle/adipose tissue; smaller than chylomicrons --> higher density; HAS APO B100 vs low protein, high fat (chol + chol-esters) => low density; made from VLDL after TAG removed; deliver chol from liver to blood vs high protein, low fat => high density (smallest blood lipoprotein); deliver chol from blood to liver or esterify chol via LCAT to IDL vs as VLDL loses TAGs, they become intermediate density lipoproteins => smaller and higher protein --> high density --> IDL taken up by liver to become LDL or HDL

Answer 42

recognizes apoE and apoB100 --> binds V/LDL, HDL, IDL, chylomicrons and bring them into cell by endocytosis to deliver chol/esters. receptor mediated process: endosome fuse w/ lysosome --> lipoprotein degraded to chol --> some chol move to ER or re-esterified to minimize chol in cell --> receptors = recycled to Golgi to plasma membrane

Answer 43

in liver and intestine; apoA-1 made and released to blood --> recruits phospholipid and chol from tissues. liver makes other proteins HDL carries --> HDL picks up chol from tissue to make chol-ester via Cholesterol Ester Transferase Protein (CETP) and puts them deep in HDL particle --> returns to liver

Answer 44

nascent HDL made in liver and intestine --> HDL picks up chol in tissue --> chol = esterified via LCAT and moved to interior of HDL particle --> chol-esters can be converted to LDL or delivered to liver

Answer 45

yes in the blood; they provide apoproteins apoC-I/II/III and apoE to nascent HDLs and nascent chylomicrons

Answer 46

minor dmg to blood vessel wall --> macs = recruited and uptake LDLs --> macs = filled w/ lipids => foam cells --> foam cells accumulate --> chemical signals induce PLT aggregation --> clot forms --> cells take up more LDL --> fat builds up --> fibroblasts excrete fibrous proteins --> cells die and leave debris --> more macs recruited --> cycle rpts until blood vessel = blocked

Answer 47

cmpds made from 20C FA; arachidonic acid = most common, prostaglandins (5C rings w/ 2x bond at C13&14), thromboxanes (6C ring, sometimes w/ O at C9 and C11), leukotrienes (3 2x bonds, sometimes w/ O bound as OH or epoxide)

Answer 48

AA bound to C2 of glycerophospholipid --> G protein receptor activated --> phospholipase A2 cleaves glycerol-FA ester at C2 --> free AA enters eicosanoid pathway w/n membrane environ vs G protein receptor activated --> phospholipase C --> IP3 --> Ca2+ enter IP3 channel in ER --> Ca2+ inc --> PLA2 --> cleaves glycerol-FA ester at C2 --> free AA enters eicosanoid pathway w/n membrane environ; if AA bound to DAG --> DAG lipase liberates it then AA goes to eicosanoid pathway

Answer 49

COX1 = constitutive enzyme in gastric mucosa, PLTs, vascular endothelium, kidneys vs COX2 = mainly expressed in macs --> inducible and made in inflamm response vs variant of COX1 --> does same fxn

Answer 50

O2 = added to AA to make 5C ring PG via COX --> PG converted to other PGs or TXs. PGH2 can be converted to TXA2 via COX in thromboxane synthesis pathway. AA = MAIN SUBSTRATE, PGH2 = MAIN PRODUCT (AA MOSTLY LEADS TO SERIES 2)

Answer 51

-OH attached to C15 vs peroxyl attached to C15 or -OH at C15 = [O] to ketone --> half life = seconds to minutes --> stops signal --> breakdown products excreted in urine

Answer 52

AA to HPETE via lipoxygenase by incorporating O2 molec to a C in a 2x bond --> HPETE = [H] to HETE, or metabolized to LT or lipoxins vs AA to epoxide --> epoxide to diHETE or HETE (prevalent in ocular, vascular, endo and renal system)

Answer 53

look at 2x bonds in nonring portion of cmpd; # of 2x bonds = # of series. dihomo-gamma-linoleic acid vs AA vs eicosapentoanoic acid; DGLA and EPA compete w/ AA binding to COX (COX favors 1 & 3)

Answer 54

mostly inhibit COX1 --> inhibit PG formation (ASA acetylate ser in active site; ibu binds competitively inhibits COX) --> dec pain/inflamm vs competitively inhibit COX --> dec pain but not inflamm. THEY STOP PG FORMATION VIA COX (IE. FREE AA CAN FORM OTHER EICOSANOIDS VIA OTHER PATHWAYS) vs inhibit PG formation by downregulating or inhibiting immune responses leading to inflamm

Answer 55

ASA covalently modifies COX1 of PLTs --> irreversibly inhibits TXA2 formation for the entire PLT life span (other NSAIDS noncovalently inhibit and will reverse as drug lvl drops)

Answer 56

weak inhibitor tho

Answer 57

in adipose and muscle (muscle has higher affinity to LPL --> use fat even if [fat] = low; adipose stores fat when [fat] = high); insulin/fed state --> protein receptor OUTSIDE of adipose/muscle cell binds to apoCII on micelle of chylomicron/VLDL --> protrudes into lipoprotein --> binds/takes TG --> TG hydrolyzed into 3 FAs and transported across membrane while glycerol goes to liver vs in adipose; glucagon/fasting --> G protein --> adenylate cyclase --> cAMP --> PKA --> HSL = phosphorylated => active INSIDE of adipose cell --> cleave TAG --> release FA and glycerol into blood --> albumin picks them up. insulin --> HSL = dephosphorylated => inactive

Answer 58

for storage; glu --> DHAP --> gly3P + FA via LPL --> TAG; can also do gluconeo to get DHAP and then make TAG from there. adipose doesn't have glycerol kinase

Answer 59

liver can't store fat; liver phosphorylates glycerol via glycerol kinase --> gly3P --> add 2 FA --> phosphatidic acid --> package it into VLDL --> go to Golgi --> released in blood --> go to adipose for storage or muscle for energy use

Answer 60

always located in membranes and myelin sheaths; NO glycerol backbone --> sphingosine backbone (palmitate + serine; palmitate w/ amino and alc group) vs sphingosine structure but amino group is amide (thanks to a fatty acid binding w/ amino group) vs 1 sugar bound to alc group vs mult sugars bound to alc group vs phosphate + N group bound to alc group

Answer 61

obesity/high TAG, inflamm, inactivity, smoking vs exer/loss of body fat, moderate alc consumption, estrogen

Answer 62

eat high sat fat --> fat malabsorption --> gallbladder doesn't ctx --> block bile release; fasting, wt cycling, and very low calorie diets inc likelihood; MNT includes high fiber, low fat, plant based diet to prevent gallbladder ctx vs acute: NPO, no enteral feeds --> IV fluids; PO feeds: low fat digestible foods, 6 sm meals/d, adeq protein and calories; if you can't start PO w/in 5-7d --> tube feeding. chronic: oral diet or tube feeding vs delayed gastric emptying d/t vol, liquids v solids, fiber, fat, osmolarity, hyperglycemia; MNT: sm freq meals, avoid high sugar meals, low fiber intake, moderate to low fat diet

Answer 63

impt for babies to digest milk fat, impt for adults to overtake bile salt fxn vs cofactor = colipase that both hydrolyze C1 and C3 of TAG to 2 free FA + 2-monoacylglycerol (more soluble than TAG) --> form mixed micelles w/ bile salts; hydrolyzes all FA chain lengths vs removes FA esterified w/ other cmpds (ex: chol-esters)

Answer 64

contain chol, fat-soluble vit, monoglycerides, phospholipids, bile acids; travel to apical membrane of enterocytes; products of fat digestion enter cell by simple diffusion. TGs = remade (2 free FA + 2-monoacylglycerol) in SER, apoB48 made in RER --> micrsomal triglyceride transfer protein (MTTP) attaches TAG to apoB48 --> goes to Golgi --> TAG packaged to chylomicrons for transport thru lymph to thoracic duct (bypass liver)

Answer 65

FA, TG, wax vs phospholipids (sphingomyelins, plasma membrane), glycolipids, lipoproteins. energy prod, fat storage, structure like cell membrane, cofactors like vit

Answer 66

avoid added sugars vs choose right carbs to feel fuller vs dietary fibers = preventative effect vs bind to fat soluble carcinogens and remove them from gut

Answer 67

coupled transport of glucose and galactose into cell

Answer 68

gluconeo fails

Cell Bio 3 Flashcards

(93 cards)