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70 Cards in this Set

  • Front
  • Back
Ketones
-Thiolase
-HMG-CoA synthase
-HMG-CoA lyase
-Acetoacetate dearboxylase
or
-Hydroxybutyrate dehydrogenase
-------Only made wehn CAC is stopped and Acetyl CoA is building up
-------Can be converted back up same intermediates to Acetyl-CoA
are not oxidized in the liver
Propionate to Succinyl CoA
3 carbon
-Carboxylase
-Methyl malonyl CoA racemase
-Methyl malonyl CoA mutase
----B12
Pathways turned on by
-ADP
-AMP
-NAD+
Pathways turned off by
-ATP
-NADH
Cyanide
Blocks complex 4
-everything up to there reduced
-nothing pumped through because nothing to oxidize
Uncouplers
No gradient
--no ATP
--no O2
lets heat off (adipose)
oligomycin
inhibits ATP synthesis
-no ATP
-O2 consumed
ionophore
no ATP
O2 consumed
retenon
inhibits complex 1
-no ATP
-O2 not consumed
Antimycin
inhibits complex 3
-everything 'backs' up
-nothing made/consumed
Glutathione
GSSG (reduced)
-gets rid of hydrogen peroxide
-recycled by glutathione reductase
---------NADPH --> NADP+
Glucose 6P dehydrogenase
NADP+ --> NADPH
--if problem, unhealthy RBC
PPP
in cytosol
Nicotinamide nucleotide transhydrogenase
makes NADPH in mitochrondria (becuase no PPP)
Brached FA
-can't get into mito
Conjugated FA
have to be reduced with NADPH-->NAPD
Unsaturated FA
-Acyl-CoA dehydrogenase (FAD)
------has to be trans (isomerase to made trans)
-enoyl-CoA hydratase
-dehydrogenase (NADH)
-thiolase (input CoASH)

approx 4ATP for every Acetyl CoA formed
9 ATP for every pass around the CAC

Branched the same except cleaved to the 3 carbon (propionly carbon)
Carnitine acyl transferase I
-Acyl CoA + carnitine in the cytoplasm
-enterance through the shuttle is the rate limiting step
FA > 12 Carbons have to undergo transport, those 12 or less diffuse
Carnitine acyl transferase II
-Acyl CoA liberated in the mitochondria
pyrophosphatase
cleaves PP
Acyl-CoA Synthetase
puts the the CoA onto a lipid
hydroxyl radical
not dangerous
-damages lipids and DNA proteins
respiratory burst
HOCl to kill bacteria
can lead to OH however
Glycerol 3P Shuttle
Cytosolic NADH = 1.5 ATP
-comes in at complex 3 through Q
from glycerol 3P --> dihydroxyacetone phosphate
------by dehydrogenase
Ubiquinone (Q)
carries electrons between Complex one, two, and the cytosol shuttle
ETC
-no energy is used to make ATP
-energy to push ATP out of active site (about 4H+ to yeild one ATP)

NADH = 2.5 ATP (10 H+)
FADH2 = 1.5 ATP (6 H+)
-------enter at complex 2
oxidase
O2 is the electron acceptor but O atoms are not in product
oxygenase
O is directly incorporated
phosphate translocase
inorganic P against gradient by H+ gradient
ATP synthase
H+ to the matrix from mitochondria
can be driven by charge difference (low [H+] and high pH)
malate-aspartate shuttle
cytosolic NADH = 2.5 ATP
goes into complex one
Calvin cycle
plants use FA for glucose
RUBISCO rate limiting enzyme
PPP
regulated at glucose 6P
---NADP --> NADPH with Mg and a degydrogenase to lactone
eventually to ribose 5P
transketolase
in the PPP
transfers the top two carbons
no energy to regernerate into glucose or fructose 6P
transaldolase
in the PPP
transfers the top three carbons
no energy to regernerate into glucose or fructose 6P
increasing beta oxidation
increases ketone body formation
Cholesterol Synthesis
HMG-CoA Synthase
HMG-CoA reductase to mevalonate
C5 -- C10 -- C15 -- C30 -- steriod
HMG-CoA reductase
regulated step
denatured by cholesterol
cholesterol also destablizes the mRNA
phosphorylated by insulin
ceramide
makes shpingomyelin
makes glycoshingolipids and gangliosides
surfactant
comes from alveolar type II cells
makes a monolayer inside the alveolar sac to make sure they stay open and interfer with h bonding
Statin class of drugs
inhibits HMG-CoA reductase
malic enzyme
produces NADPH and pyruvate
lipoprotein lipase
clips of albumin
glucocorticoids
inhitbit PEPCK in the adipose tissue which makes less TAGs
increase in PEPCK in the liver so not as mush pyruvate is made and make ketones for energy
glyceroneogenesis
controls the rate of FA released to blood
lower glyceroneogenesis = more free fatty acids because less TAG
PEP carboxylase major regulation
Pyruvate --> TAG synthesis
Palmitate
16:0
Stearate
(18:0)
Palmitoleate
16:1
Oleate
18:1
Linoleate
18:2
plants are the only ones who make so is essentail FA
same with alpha linoleate (18:3)
Arachidonate
(20:4)
Synthesis FA
desaturation (NAPDH -- NADP)
Elongation
desaturation
Arachidonate
to leukotriens
--- with lipoxygenases
PGH2
Synthesized with COX 1,2,3 and GSH
pain relievers block COX enzymes
Citrate transporter
gets the acetyl-CoA into the cytosol from the matrix
citrate lyase
frees acetyl-CoA into the cytosol for FA synthesis
malonyl CoA
Biotin carrier
--- uses actyle CoA (biotin) carboxylase with ATP - ADP
--- next an input of acetyl-CoA with a transcarboxylase
--inhibits carnitine acyl transferase I because you don't wnat pieces being shipped into matrix for breakdown
FA synthase complex
puts acetyl CoA on first
next the malonyl CoA
---both free up CoASH
added in 2 units with a loss of CO2 each time until Palmitate
condensation (CO2 leaves)
reduction (NADPH - NADP)
dehydration (H2O leaves)
reduction (NADPH - NADP)
translocation and ready for the next malonyl CoA
thioesterase
the enzyme that clips off FA in shorter chains than palmitate in mammary glands
---regulated by hormones
high insulin
makes acetyl CoA
which upregulates acetyl CoA carboxylase
which makes more free fatty acids
which makes more TAGs for storage
citrate
shows cells have energy
activates acetyl CoA carboxylase
Acetyl CoA carboxylase
major control of FA synthesis
glucagon and epinephrine inhibit (phosphorylation = inactivation)
palmitoyl CoA allostericall inhibits this enzyme
albumin
carries FA and glycerol
TAGs
dihydroxyacetone (liver and adipose) (NADH - NAD) to glycerol 3P
gylcerol by gylcerol kinase (liver) (ATP-ADP) to glycerol 3P
glycerol 3P
acyl transferases to add FA onto carbons 1 and 2 with freeing of CoASH
(FA synthisized by the FA synthase complex and CoASH added by and acyl CoA synthetase)
makes diacylglycerol 3P (phosphatidic acid)
phosphatidic acid
phosphate taken off by a phosphatase and 1,2 diacylglycerol forms
another FA-CoAsh added with freeing of the CoASH
TAGs synthesized in
the cytosol in the liver (smooth ER)
then packages and sent as VLDL
ceramide
precusor to all othe sphingolipids
usually 20-22 c long
acts as an antifreeze and helps in embryo development
LDL
cholesterol inhibits LDL receptos
(these bind and loose cholestorol to the cell)
exo-gylcosidase
enzymes that cleave sugars off of the ceramide-sphingolipid structures
problems in cleaving the beta links