Overall Things I Keep Getting Wrong Flashcards
Mnemonic for heme sythesis
Ala pros hyd meth under corporations power houses
Where does lead poisoning act
It inhibits
Ala dehydratase enzyme so you’ll have a build up of ala
And
Ferrochelatase
Competes with ca2+
What does glycogen phosphorylase need
PLP
Which end of glycogen does glycogen phosphorylase attack
Non reducing end
Glycogen phosphorylase when its phosphorylated
ACTIVE
FAST state
Glycogen synthase when its NOT phosphorylated
ACTIVE
FED state
Symptoms of acute intermittent porphyria
5 P’s
Painful abdomen
Port wine urin
Polyneuropathy
Psychological disturbances
Precipitated by drugs alcohol and starvation
How do you treat AIP
Glucose and heme
Most common porphyria inhibits what enzyme
Uroporphyrinogen decarboxylase
What path is G6P dehydrogenase apart of
PPP
Malate to OAA makes and conversely
NADH
OAA to malate uses NADH
What pathway is pyruvate dehydrogenase in/ what does it do
Pyruvate——>Acetyl CoA
TCA
What pathway is pyruvate carboxylase apart of what does it do
Pyruvate —>OAA
TCA
GNG
What does pyruvate carboxylase need with it
CO2
ATP
Biotin
Alanine aminotransferase does what and where
Pyruvate<—>alanine
Cytoplasm
Acetyl can go to make
FA
Cholesterol
TCA cycle
Pyruvate<-?->lactate
Where
Lactate dehydrogenase
Cytoplasm
RBC
During strenous muscle activity
What does pyruvate<—>lactate make
regenerates NAD+
what can inhibit pyruvate dehydrogenase
NADH from FA
First barrier to cross in GNG all the enzyme names
Pyruvate —pyruvate carboxylase—> OAA
OAA —PEP carboxykinase—>PEP
If it goes
pyruvate > OAA —malate dehydrogenase—> malate
Fructose 1,6 bisphosphate -?-> fructose 6 phosphate
And vice versa
Fructose 1,6 bisphosphatase
PFK1
Glucose 6 phosphate -?-> glucose
And vice versa
Glucose 6 phosphatase
Hexokinase/glucokinase
Glucose 6 phosphatase and fructose 1,6 bisphosphatase are both
Inducible by glucagon
Glucose 6 phosphatase is used where
GNG and glycogen pathway
Tyrosine effects with def in dihydrobiopterin reductase or dihydrobiopterin synthetase
Decreased catecholamines
Tyrptophan effects with def in dihydrobiopterin reductase or dihydrobiopterin synthetase
Decreased serotonin
Trigger for all alcohol problems
Excess NADH
How does NADH inhibit TCA cycle
Inhibits is citrate dehydrogenase
And
Inhibits α-ΚG dehydrogenase
And
It favors the production of Malate NOT OAA
When NADH is high from drinking which does it favor OAA or Malate
What does this result in
Malate
Results in decreased GNG = hypoglycemia
Why do alcoholics have lactic acidosis
Bc their body has way too much NADH so it needs to regenerate more NAD+. IT does this by utilizing pyruvate>lactate path bc this takes NADH and makes NAD+. The result is a ton of lactate
What is an activator of acetyl CoA carboxylase and what does it do
Citrate is an activator
Acetyl-CoA —-acetyl CoA Carboxylase—> malonyl CoA—— β oxidation
What does insulin do in the adipose tissue
Dephosphorylation of pyruvate dehydrogenase and lipase in adipose tissue
What does insulin do in muscle
Dephosphorylates glycogen synthase and glycogen phosphorylase
Glycolysis RLE
PFK1
GNG RLE
Fructose 1,6 bisphosphatase
TCA RLE
Isocitrate dehydrogenase
Glycogen synthesis RLE
Glycogen synthase
glycogenolysis RLE
Glycogen phosphorylase
HMP shunt RLE
Glucose 6 phosphate dehydrogenase (G6PD)
De novo pyrimidine sythesis RLE
Carbamoyl phosphate synthetase II
De novo purine sythesis RLE
Glutamine PRPP amidotransferase
Aka
AMIDOPHOSPHORIBOSYL transferase
Urea cycle RLE
Carbamoyl phosphate synthetase I
Fatty acid sythesis RLE
Acetyl CoA carboxylase (ACC)
Fatty acid oxidation RLE
Carnitine acyltransferase I
Ketogenesis RLE
HMG CoA synthetase
During ketogenesis you can have a lot of KiSs chocolate
Cholesterol sythesis RLE
HMG CoA reductase
She you make a lot of cholesterol you’re fat and angry and you “see (C) Red”
β cells release what vs α cells
β = insulin
α = glucagon
Glucagon has an a so glucagon is alpha
When you’re fasting what is increasing
Glucagon
Triglyceride hydrolysis
Glycogen degration
GNG
KB production
Release of AA
When you are fed what is being synthesized
Triglycerides
Glycogen
FA
VLDL
Protein - replenish any protein degraded during previous post absorptive period
When you see insulin think
DEPHOSPHORYLATION by activating phosphatase
Which enzymes does insulin work INdirectly on what do they do
PFK2 and fructose 2,6bisphosphatase
Increases level of fructose 2,6 bisphosphate which activates PFK1 and continues glycolysis
When you see glucagon think
PHOSPHORYLATION by PKA (protein kinase)
What are they key enzymes glucagon phosphorylates
Pyruvate kinase
Glycogen sythase
Glycogen phosphorylase
Acetly CoA carboxylase
What + activates PEP>Pyruvate
Fructose 1,6 bisphosphate
What do insulin and glucagon act on in β oxidation
Hormone sensitive lipase
glucagon receptor is what and what does it do
G protein coupled receptor
Increases adenylate cyclase
Which turns ATP to cAMP
Which activates kinase a
Which PHOSPHORYLATES
Insulin receptor is what and what does it do
Tyrosine kinase receptor
It triggers protein phosphatases
Which will DEPHOSPHORYLATE
What are all the enzymes in FA synthesis insulin induces and which are the ones that have a special function
Malic enzyme - NADPH
G6PDH - increase NADPH
FA sythase
Acetly CoA carboxylase
Citrate lyase
LPL in response to insulin and glucagon and why
Insulin increases it in adipose BC we want to break down triglycerides into FA for storage
Glucagon decreases it in adipose BC we don’t want that
Fight of flight in the liver vs skeletal muscle
Liver will have phosphorylation of PFK2 and F2,6bisphosphatase. The result is to decrease glycolysis here and increase GNG.
Muscle will have phosphorylation of PFK2 and F2,6 bisphosphatase. This will result in an increase of glycolysis here.
