Exam 2 -- questions Flashcards
where does heme synthesis occur
partly in mitochondria, partly in cytosol of liver and bone marrow
where does fa degradation occur
cytosol–>mitochondria
where does gluconeogenesis occur
first part in mitochondria, then in cytosol. (last step only possible in liver)
where does PPP occur
liver, adrenal cortex, lactating tissues, RBCs
PTL vs LPL vs HSL
PTL: dietary TG to MAG and glycerol
LPL: TGs in CMs to MAG and glycerol for adipocyte take up
HSL: hydrolyzes adipocyte TG to free fa’s
CM vs VLDL vs LDL vs HDL
CM: dietary TGs in small intestine–>tissues
VLDL: endogenous TGs in liver –> tissues
LDL: made from depleted CM/VLDL, goes to tissues, only one that enters cells (receptor mediated endocytosis)
HDL: returns tissue chol to liver for degradation
how are odd chain fa broken down?
propionyl CoA (3C) –> succinyl CoA. uses cofactors biotin and B12. Uses ATP.
how much energy is obtained in ONE round of beta-oxidation?
make 1 FAD --> 2 ATP make 1 NAD --> 3 ATP make 1 ACoA --> 12 ATP lose 2 ATP in making acyl-CoA total= 15 ATP
what are the lipogenic enzymes:
- ACoA carboxylase
- fa synthesis
- citrate lyase
- malic enzyme
- dehydrogenase in PPP
how/where does fa chain elongation occur?
- ER membrane
- acyl-Coa donates 2C units to carboxy terminus of malonyl CoA
how/where are double bonds added into fa’s?
- ER membrane
- accomplished by desaturases (9, 6, 5)
sphingolipid synthesis pathway
All derived from sphingosine.
Sphingosine
(+fa) = ceramide
(+phosphotidyl choline) = sphingomyelin
OR ceramide + carb = glycosphingolipid
(Kaiser 5)
cellular control of chol synthesis?
inc chol activates protease, protease releases SREBP from ER, goes to nucleus to activate SRE. SRE now activates HMGCoa and LDL receptor production
KB synthesis pathway
2 ACoA –> acetoacetyl CoA –>3-hydroxy-3-methyl-glutaryl CoA –>acetoacetate–>acetone or 3-hydroxybutyrate
leptin vs ghrelin
leptin: produced by adipocytes, dec appetite, inc caloric expenditure
ghrelin: produced by stomach, inc appetite
10 essential aa’s
PVT TIM HALL
phe, val, thr, trp, ile, met, his, arg, lys, leu
negative vs positive N balance
Positive : taking in more than you’re excreting, growing/healing etc
CPS I vs CPS II
Both make CP
CPS I in mito during urea cycle
CPS II in cytosol during pyrimidine synthesis
how does NH4 get transported into bloodstream/liver for degradation?
- most is glutamine
2. from muscles as alanine (pyr + NH3)
which are the 2 ONLY ketogenic aa’s
Leu and Lys
how is THF made
folate to dihydrofolate to THF. Both steps need DHFR (dihydrofolate reductase). This is what methotrexate blocks!
how are dNTPs made from NTPs? ie how to make deoxyribose nt’s from ribose nt’s?
ribonucleotide reductase. Blocked by binding of dATP (adenosine deaminase deficiency)
Complex carb: proteoglycan. where is it made
protein w long repeating dissacharide units (GAG)
“slippery,” has shell of water
made in golgi
form ECM, or found in synovial fluid, eye, cartilage, mucous
complex carb: glycoprotein. where is it made
protein with shorter oligosaccharide, usually branched
made in RER and golgi
found in ECM, cell surface, functions for cell recognition, antigenicity, globular proteins of human plasma
direct reversal of DNA damage
photolyase- e coli / plants. undoes uv damage
and
AGT (or MGMT)- not in plants, directly removes methyl group that was the mutation
MMR
identify methylated (older/parental) strand and fix errors on daughter strand according to old
BER
repairs base alteration or loss. glcosylase recognizes/removes error leaving AP site. Filled in by AP-endonuclease
NER. what are diseases assoc?
UV specific endonuclease, recognizes thymine dimers and cuts it out via “double incisions”.
**XP, Cockayne’s, Trichothiodystrophy
HR (also called recombination repair). what disease is assoc w this?
used to repair ds breaks.dna repaired from undamaged sister xsome. strands joined via holliday junction, branch migration and resolution.
**BRCA
Nonhomologous end-joining (NHEJ)
used to repair ds breaks. dna ends processed and ligase joins the 4 ends, more error prone, some dna lost
catecholamine synthesis pathway? what deactivates these/or inactivates the deactivation (drug)?
tyr–>dopa–>dopamine–>norepi–>epi. MAO inactivates, MAO inhibitor will increase life of NT
serotonin synthesis
try–>5-hydroxytryptophan–>serotonin.
define heritability
proportion of observable diff in trait bw individuals within population due to genetic differences
allelic vs locus heterogeneity
allelic: different mutations at some locus/gene cause disease
locus: multiple genes w mutations lead to “same” disease
