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FSHN 470- Unit 3
| Question | Answer |
|---|---|
| 3 common ROS | superoxide (O2-), hydroxyl OH-, perhydroxyl OOH- |
| 5 sources of radicals | activated macrophages, NO synthase, ionizing radiation, transition metals + oxygen, oxidation of reduced flavins |
| ROS chain reaction | R- created from OH-, then another one is made at end and reaction repeats |
| PUFA oxidation | very stable b/c of resonance stabilization |
| why don't radicals form on saturated or monounsaturated? | unstable & revert back to starting product |
| why is lipid peroxidation of membranes bad? | -OOH push bilayer apart & makes them leaky (ions get back in) |
| LDL oxidation | apo B100 + charges go away, then must be picked up my macrophages instead of binding to receptor |
| oxyradicals and cancer | OH- and ROO- activate many signaling pathways involved in gene expression/cell growth |
| SOD is __ dependent | Cu and Mn |
| cytoplasmic SOD | Cu dependent, and Zn structural role |
| extracellular SOD | Cu dependent |
| mitochondrial SOD | Mn-dependent, functions and expressed only in the mitochondria |
| ferric iron | Fe3+ |
| ferrous iron | Fe2+ |
| glutathione | tripeptide in all cells in high conc; (glutamate, cysteine, glycine) *abbreviated as GSH (SH provides reducing equivalents) |
| glutatione peroxidases | quenches H2O2 and FFA hydroperoxides |
| three types of GSHPx | cytoplasmic (H2O2/FFA hydroperoxides), plasma, phospholipids |
| GSHPx's are different in ___, but same in that ___ | they come from different genes (distinct enzymes), they require Se as a cofactor |
| where is Selenium toxicity seen? | American west from locoweeds |
| where does regeneration of vitamin E occur? | interface of aqueous and lipid portion of cells (due to different solubilities) |
| why should you not take excess vitamin C? | it's a pro-oxidant in excess |
| how does vitamin C help protect LDL from oxidation? | re-generates vitamin E, which intercepts radicals of LDL |
| phytonutrients | many are antioxidants and intercept free radicals similar to how vitamin E functions |
| what are the 4 human desaturases? | Δ9, Δ6, Δ5, Δ4 |
| regulation of desaturases & elongases | NO PHOSPHORYLATION, response element (when fed) |
| which desaturase is the most responsive to fasting/feeding? | Δ9 |
| 2 essential fatty acids | linoleic & a-linolenic |
| does n-6 consumption affect tissue arachidonic acid? | no, plateaus at 2-3% of kcal |
| what is made if n3 is deficient? | DPA |
| what is made if both n3 and n6 are deficient? | mead acid (Δ6 desaturated, 2C elongation, Δ5 desaturation of oleic acid) |
| major product of n-3 FAs | DHA (very little EPA), but only 1% conversion from n-3 to these |
| regulation of n-3/n-6 pathways by insulin | increases expression of Δ6 and Δ5 |
| which step in n-3/n-6 pathway is limiting? | Δ6 desaturase (1st step) |
| how can Δ6 and Δ5 desaturases be down-regulated? | high PUFA in the diet |
| US ratio of n-6/n-3 | 10:1 (4:1 before increased use of vegetable oils in 1950s) |
| optimal ratio n-6/n-3 (paleonutritionists) | 2:1 or 3:1 |
| major source of DHA in Americans | chicken |
| does diet linolenic acid affect phospholipid DHA? | not significantly- must eat EPA and DHA (they also decrease phospholipid AA) |
| are people deficient for n-3? | no, health conditions just improve with increased intake of them! |
| linoleic acid AI | ~15g *no AI for AA b/c not essential |
| linolenic acid AI | ~1.5g *no AI for EPA/DHA b/c not essential |
| eicosanoids produced where? | locally (paracrine)- mostly from AA |
| what do eicosanoids do? | normal & inflammatory states |
| arachidonic acid gives rise to | group 2 prostanoids, leukotrienes, and lipoxins |
| linoleic acid gives rise to | group 1 prostanoids and leukotrienes |
| a-linolenic acid gives rise to | group 3 prostanoids and leukotrienes |
| cyclooxygenase makes __ | prostanoids and thromboxanes |
| lipoxygenase makes ___ | leukotrienes and lipoxins |
| what is the common intermediate for all prostaglanins? | PGH2 |
| PGH synthase | (aka COX); 2 domains; COX (adds 2 O2), peroxidase (reduces PGG2 to PGH2) |
| half-lives of PGs | degrades in seconds or quickly degraded by kidney/lung enzymes |
| COX-1 isoform of PGHS | constitutive isozyme; always present; expressed in all cells (housekeeping fxns) |
| COX-2 isoform of PGHS | inducible isozyme, inflammatory signals |
| EPA dietary effects | PGHS has low affinity for EPA; so enriches phospholipid EPA & displaces PL AA; small increase in 3-series PG |
| DHA dietary effects | only effect is to displace AA from PLs |
| TXA2 | platelet PG (atherogenic) |
| PGI2 | endothelial cell PG (anti-atherogenic) *counters TXA2 |
| GI cancer and PG | colon cancer proliferates by PGE2-dependent processes, if block COX2, blocks colon cancer |
| osteoarthritis PG | inflammatory cytokines -> COX2 production of PGE2-> collagen degradation->osteoarthritis |
| regulation of COX2 | n-3 PUFA block expression of COX2 via SREBP |
| NSAIDs inhibit | both cox1 and cox2 |
| first NSAID | acetylsalicylic acid (aspirin) |
| how does aspirin work? | acetylates COX1 at a serine (inhibits it), stops COX2 activity (no PGH2 made), acetylated COX2 produces signaling molecules from EPA/DHA |
| acetaminophen | doesn't relieve inflammation, but few side effects |
| ketoprofen/naproxen | 8 hour pain relief (NSAID) |
| voltaren | arthritis- more specific for COX2- fewer GI problems |
| COX2 inhibitor problems | excess CVD deaths from these |
| COX2 CVD | does nothing to TXA2 (which is prothrombic) decreases PGI2 (which is a vasodilator) |
| low dose aspirin | enough to decrease TXA2, but not enough to decrease PGI2 (significantly) |
| SCOT | (ketolytic tissues) converts acetoacetate to acetoacetyl-coA |
| 2 regulatory enzymes in ketone metabolism | SCOT and HMGCS2 |
| HMGCS2 regulation | activated by glucagon, inhibited by insulin and succinyl co-A |
| SCOT regulation | inhibited by insulin and transcription factors |
| ketogenesis helps with what? | prevents accumulation of incompletely oxidized FA intermediates, provides energy substrates in glucose-limited states in low CHO high FA conditions |
| how does liver switch to produce ketone bodies? | less OAA b/c of gluconeogenesis, so can't use TCA; FFA inhibits pyruvate kinase and acetyl coA in mitochondria inhibits pyruvate dehydrogenase |
| is ketone body regulation increased by FFA coming to liver? | no- KB would increase from exercise/stress which does not occur |
| NADH and ketones | as NADH increases, so does beta hydroxy butyrate, which goes to blood; if NADH drops, acetoacetate goes up, which will be converted to acetoacetyl coA and shut down KB production |
| what enzyme(s) transfer NH2 group to another alpha-keto acid? | aminotransferases |
| what enzyme converts NH2 to NH3? | glutamate dehydrogenase |
| which 3 amino acids cannot be transaminated? | lysine, threonine, and proline |
| which vitamin activates transaminases? | B6 (pyridoxine) |
| what is the only ketogenic amino acid? | leucine |
| what makes an amino acid glycogenic? | 3 or more carbons for gluconeogenesis |
| how many ATPs are needed to break down 1 NH4? | 4, but NADH is made so only 1 |
| carbamoyl phosphate synthase 1 regulation | (1st enzyme of urea cycle- in gut) n-acetyl glutamate (from glutamate)= positive allosteric effector |
| ornithine transcarbamoylase | (2nd enzyme of urea cycle- in gut) ornithine controls flux |
| long term urea enzyme regulation | (ornithine transcarbamoylase) 5x increase after 4-8 days; mechanism is probably transcription or translation |
| 60% of AA in muscle are | alanine and glutamine |
| most nitrogen into urea cycle can also come from (& what enzyme?) | purine metabolism; AMP deaminase |
| only __ has all 5 urea cycle enzymes | liver (gut has ornithine transcarbamoylase and carbamoyl phosphate synthase) |
| feasting: increased ornithine in the liver does what? | increases flux through urea cycle via Km effects |
| gut is the key to urea cycle why? | citruline from gut increases liver ornithine, increased flus thru urea cycle |
| pentose phosphate | ribose 5- phosphate -> nucleotides + NADPH |
| alanine's alpha keto acid | pyruvate |
| aspartate's alpha keto acid | oxaloacetate |
| glutamine is used as | an energy substrate |
| branched chain AA use | fat storage, nitrogen |
| aromatic AA use | tryptophan converted to serotonin in the brain |
| glucose & ketone use starvation day 3 vs 30 | 3: 2x as much glucose as ketones; 30: 2x as many ketones as glucose |
| adipose & muscle use starvation day 3 vs 30 | 3: 2-3x adipose as muscle 30: 9x adipose as muscle *amt of adipose doesn't change, muscle just goes down |
| fuel output of liver starvation day 3 vs 30 | 3: 1:1 ratio glucose and ketones 30: 2x ketones than glucose |
| other effects of trauma (2 hormones) | water retention from ADH; sodium retention from aldosterone |
| how is BAT different than WAT? (4) | high lipid content, small lipid droplets, more vascularized, more mitochondria |
| protein that permits H+ flux w/out ATP production | thermogenin aka UCP |
| higher BAT in which gender? | women |
| mass of BAT correlates inversely with | BMI |
| what mineral is required for T3 and T4 in BAT? | iodine |
| sleeping BAT study | 19C (66F)-> higher DIT and insulin sensitivity (reversible w/ higher temps) |
| white adipose comes from (2) | endothelial precursor or WAT precursor |
| brown adipose comes from (2) | muscle satellite cell or BAT precursor |
| difference b/w beige and brown adipocytes | beige come form white; BAT different origin |
| which eicosanoid is involved in osteoarthritis and colon cancer? | PGE2 |
| HMGCS1 vs HMGCS2 | 1: HMG Co-A for cholesterol synthesis 2: HMG Co-A for acetoacetate |
Created by:
melaniebeale
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