Flashcards in metabolism Deck (91):
metab that occurs in mito
fatty acid BETA-ox.
acetyl co-A prod.
metab that occurs in cytoplasm
protein synth (RER).
steroid synth (SER).
metab that occurs in both mito and cyto
HUGS take two.
use ATP to add high-energy phosphate onto substrate
adds inorganic phosphate onto substrate without using ATP
removes phosphate group from substrate
transfers CO2 groups with help of BIOTIN
rate-determining enzyme: glycolysis
rate-determining enzyme: gluconeogenesis
rate-determining enzyme: TCA cycle
rate-determining enzyme: glycogen synthesis
rate-determining enzyme: glycogenolysis
rate-determining enzyme: HMP shunt
rate-determining enzyme: de novo pyrimidine synth
carbamoyl phosphate synthetase II
rate-determining enzyme: de novo purine synth
rate-determining enzyme: urea cycle
carbamoyl phosphate synthetase I
rate-determining enzyme: fatty acid synth
acetyl-coA carboxylase (ACC)
rate-determining enzyme: fatty acid oxidation
carnitine acyltransferase 1
rate-determining enzyme: ketogenesis
rate-determining enzyme: chol synth
aerobic metab of glucose produces?
32 ATP: malate-aspartate shuttle in heart, liver.
30 ATP: glycerol-3-phosphate shuttle in muscle.
anaerobic glycolysis produces?
2 net ATP per glucose molec
activated carrier of phosphoryl
activated carrier of electrons
activated carrier of acyl
activated carrier of CO2
activated carrier of 1 carbon units
activated carrier of CH3 groups
activated carrier of aldehydes
TPP (thiamine pyrophosphate, B1)
universal electron acceptor: NAD+
from vit B3.
used in catabolic processes to carry reducing equivalents away as NADH.
universal electron acceptor: NADP+
NADPH made in HMP SHUNT.
used in anabolic processes as a SUPPLY of reducing equivalents.
universal electron acceptor: FAD+
from vit B2.
processes that use NADPH
1. anabolic processes: steroid and FA synth.
2. respiratory burst.
4. glutathione reductase.
phosphorylate glucose to yield GLUCOSE-6-PHOSPHATE.
1st step of glycolysis AND glycogen synth in liver, depending on enz location.
high affinity (low Km).
low capacity (low Vmax).
NOT induced by insulin.
what inhibits hexokinase?
glucose 6-phosphate via feedback inhib
LIVER and BETA CELLS of pancreas.
low affinity (high Km).
high capacity (high Vmax).
induced by insulin.
what does glucokinase with excess glucose?
phosphorylates it (after a meal) to SEQUESTER it in the liver - liver serves as blood glucose buffer
which steps in glycolysis require ATP?
what inhibits glucokinase?
what inhibits PFK1?
what stimulates PFK1?
which steps in glycolysis produce ATP?
1. phosphoglycerate kinase.
2. pyruvate kinase.
what inhibits PK?
what stimulates PK?
fructose bisphosphatase 2
active in FASTING state:
increase glucagon = cAMP = protein kinase A = increase fructose bisphosphatase 2.
F26BP to F6P for gluconeogenesis.
decrease PFK2 = less glycolysis.
active in FED state:
increase insulin = decrease cAMP = decrease protein kinase A = increase PFK2.
F26BP stimulates PFK1 for more glycolysis.
decrease fructose bisphosphatase 2.
pyruvate dehydrogenase complex RXN
pyruvate + NAD+ + CoA =
acetyl coA + CO2 + NADH
pyruvate dehydrogenase complex COFACTORS
1. TPP (B1)
2. FAD (B2)
3. NAD (B3)
4. CoA (B5)
5. lipoic acid
what activates pyruvate dehydrogenase complex?
increased NAD+/NADH ratio.
what other complex is similar to pyruvate dehydrogenase complex?
alpha-ketoglutarate dehydrogenase complex in TCA cycle. same cofactors, similar substrate.
alpha-KG --> succinyl CoA.
what inhibits lipoic acid?
arsenic - cause vomiting, pain, rice water stools, garlic breath, delirium.
TX of arsenic poisoning
dimercaprol (chelator) to displace arsenic ions
pyruvate dehydrogenase deficiency
back up of substrate (pyruvate, alanine).
increased LDH activity to regenerate NAD+ causes LACTIC ACIDOSIS.
can be congenital or
acquired (alcoholics, B1 def).
findings in pyruvate dehydrogenase deficiency
TX of pyruvate dehydrogenase deficiency
increased intake of KETOGENIC nutrients-
high fat content or
increased Lysine and Leucine (the only purely ketogenic AAs)
pyruvate can be metabolized into:
3. acetyl CoA.
function of alanine from pyruvate
carries amino groups from muscle TO LIVER
function of oxaloacetate from pyruvate
replenish TCA cycle or
used in gluconeogenesis
function of acetyl CoA from pyruvate
transition from glycolysis to TCA
function of lactate from pyruvate
end of anaerobic glycolysis
which organs use anaerobic glycolysis (and thus produce lactate)?
what inhibits pyruvate dehydrogenase?
irreversible enzymes in TCA
1. pyruvate dehydrogenase.
2. citrate synthase.
3. isocitrate dehydrogenase.
4. alpha-ketoglutarate dehydrogenase.
intermediates in TCA (in order)
"Citrate Is Kreb's Starting Substrate For Making Oxaloacetate"
NADH electrons enter mito...
or glycerol-3-phosphate shuttle.
where does FADH2 enter ETC/oxphos?
complex II (at lower energy level than NADH)
ATP produced by ATP synthase
using proton gradient formed in intermembranous space.
1 NADH = 3 ATP.
1 FADH2 = 2 ATP.
ox phos poison: electron transport inhibitors
directly inhibit ETC, causing decreased proton gradient and block of ATP synth.
3. antimycin A.
ox phos poison: ATP synthase inhibitors
directly inhibit mito ATP synthase, causing increased proton gradient.
NO ATP IS PRODUCED bc electron transport stops.
ox phos poison: uncoupling agents
increase permeability of membrane, causing decreased proton gradient and increased O2 consumption.
ATP synth stops but ETC continues.
2. aspirin (overdose).
3. thermogenin (brown fat).
gluconeogenesis occurs in?
enzymes also found in kidney, intestinal epith.
gluconeogenesis irreversible enzymes
"Pathway Produces Fresh Glucose"
deficiency of gluconeogenesis enzymes leads to?
why cant MUSCLE participate in gluconeogenesis?
it lacks glucose-6-phosphatase
what type of FA can also contribute to gluconeogenesis?
odd-chain FA: yield 1 propionyl CoA during metabolism, which can enter TCA as succinyl CoA and undergo gluconeogenesis.
*even-chain FAs only yield acetyl CoA equivalents
pyruvate to oxaloacetate.
requires biotin, ATP.
activated by acetyl CoA.
oxaloacetate to PEP.
fructose-1,6-bisphosphate to fructose-6-phosphate.
glucose-6-phosphate to glucose.
key role: provide NADPH from abundant G6P supply.
aka pentose phosphate pathway.
phases of HMP shunt
1. oxidative (irreversible).
2. nonoxidative (reversible).
products of HMP shunt
3. glycolytic intermediates (G3P, F6P).
sites of HMP shunt
lactating mammary glands.
liver, adrenal cortex (FA/steroid synth).
RBCs (glutathione reduction).
ATP in HMP shunt
none used or produced
oxidative rxn of HMP shunt
yields 2 NADPH, CO2, ribulose-5P
(multiple in-between steps)
via G6P dehydrogenase.
nonoxidative rxn of HMP shunt
ribulose-5P (from oxidative phase)
yields ribose-5P, G3P, F6P
(multiple in-between steps)
via transketolase with B1 cofactor.
what enz is activated in respiratory (oxidative) burst?
NADPH oxidase -
in neutrophils, monocytes.
*NADPH involved in ROI production and neutralization
role of resp burst
immune response: rapid release of reactive oxygen intermediates (ROIs)