Metabolism Revision Flashcards
where does fatty acid synthesis occur
in the cytoplasm
what breaks down triglycerides into fatty acids and glycerol
via lipolysis (lipases)
what acitvates fatty acids
the addition of a CoA group= makes fatty acyl-CoA
what then happens to acetyl CoA
is a two carbon precursor for entry into the krebs cycle
what does carnitine allow
transport of fatty acyl into mitochondrian as fatty acyl-carnitine
what is the main storage form of lipids in the body
triglycerides
what do some lipids contain
phosphate groups, carbohydrates, proteins
can fatty acids be used for gluconeogenesis
no
are lipids mostly hydrocarbon and water insoluble or soluble
yes hydrocarbon
mostly water insoluble
lipid absorption is required for the absorption of some what
vitamins
what is the first step of fat catabolism
lipolysis
do fatty acids have to be activated for fat catabolism
no
where does activation of fatty acids occur
in the cytoplasm
what is the pathway for breakdown of fatty acids called
beta oxidation
where does beta oxidation occur
in the mitochondrian
what are the products made from each beta oxidation cycle
1 acetyle-CoA, 1 FADH2, 1 NADH + H+, 1 fatty acyl-CoA (which has been shortened by 2 carbon atoms)
how many rounds of beta oxidation occur for an even numbered saturated fat
if fat= C2n, number of oxidation cycles= n-1
how many rounds of beta oxidation will a C16 fat undergo
C16= C2n=16 carbons
16/2 -1 = 7 oxidation cycles
what will the products be for the breakdown of a C14 fatty acid
7 acetyl-CoA, 6 NADH + H+, 6 FADH2
when and where are ketone bodies formed
formed in the liver under fasting conditions
what are ketone bodies formed from
acetyl-CoA from beta oxidation
what is the role of ketone bodies
diffuse into blood stream and travel to peripheral tissues where they are important molecules of energy metabolism in the brain, heart muscle and renal cortex
important in energy production (TCA cycle) and neurotransmitter synthesis
what happens when ketone bodies are metabolised
converted back to acetyl-CoA which then enters the TCA cycle
what is the TCA cycle
stored energy is released through the oxidation of acetyl CoA
what symptom is seen when the body produces acetone
expired fruity breath
when do ketone bodies accumulate
in extreme starvation as a by product of beta oxidation
what can ketone bodies cause
ketoacidosis
where does fatty acid synthesis main occur (organ)
in the liver
what does the process of fatty acid synthesis drive
the process of lipogenesis (formation of fat)
what is used to generate acetyle CoA
glucose
what does the enzyme acetyl-CoA carboxylase do
converts acetyle CoA to malonyl CoA
what is malonyl CoA
the major fatty acid synthesis precursor
what regulates acetyl CoA activity
nutrient and energy status
where does degeneration of fatty acid occur
in the mictochondrian matrix
what reductant does fatty acid synthesis require
NADPH
what oxidant does fatty acid degredation require
NAD+, FAD
what is the maximum length of fatty acid made
C16
what increases the rate of acetyl CoA carboxylase (and therefore the rate of conversion of acetyl CoA to malonyl CoA)
citrate, insulin
what decreases the rate of acetyl CoA carboxylase (and therefore the rate of conversion of acetyl CoA to malonyl CoA)
palnitoyl CoA, AMP, glucagon, epinephrine
how does insulin regulate acetyl- CoA carboxylase
signals the fed state- stimulates the storage of fuels and synthesis of proteins
how do glucagon and epinephrine regulate acetyl CoA carboxylase
glucagon signals the staved state
epinephrine signals the requirement for energy
both mobilise glucagon stores
how does citrate regulate acetyl CoA carboxylase
stimulates allosterically- citrate levels are high when acetyl CoA and ATP are abundant
how does palmitoyl CoA regulate acetyle CoA carboxylase
is abundant when fatty acids are in excess
is fatty acid synthesis an oxidative or reductive process
reductive
what transports acetyl groups from the mitochondrian to the cytoplasm
citrate
does fatty acid synthesis require NADPH
yes
the donor molecule of carbon atoms to a growing fatty acid is
malonyl CoA
what does a lot of citrate stimulate
acetyl CoA carboxylase
what effect does the binding of citrate to acetyl CoA have
activates the catalytic effect of the enzyme
where is urea synthesised
in the liver
where does the nitrogen in urea come form
one from free ammonium, other from aspartic acid
where is the carbon in urea from
CO2
what happens to the amino group of the amino acids in the formation of urea
is removed
does removal of amino acid groups in urea formation only occur in the liver
no
can carbon skeletons of all amino acids enter the TCA cycle
yes
can glucogenic amino acids be used to form glucose
yes
can ketogenic amino acids be completely oxidised in the TCA cycle
yes
is free ammonium toxic
yes
what is the rate limiting step of glycogen breakdown
when glycogen phosporylase turns glycogen into glucose 1 phosphate
what are the two possible outcomes of glycogen breakdown
glucose formation or glycolysis
how does glucose enter the blood
GLUT2 transporter
where is glucose 6 phosphate turned into glucose
only in the liver
how does gluconeogensis proceed
via the synthesis of oxaloacetate in the mitochondrian
is gluconeogenesis energy consuming
yes
what is glycogenin and what is its role
a protein that sits at the centre of a glycogen polymer
has a catalytic activity, can covalently bind up to 4 glucose molecules to itself, essential in the formation of a glycogen polymer
what can glycogen synthase only add glucose residues to
an existing glycogen chain
where are amino acids oxidised
in the TCA cycle
what are amino acids pre cursors for
gluconeogenesis
can liver glycogen serve as a source for blood glucose
yes
can muscle glycogen be used for energy generation outside of the muscle cell
no
what must glucose be bound to before it can be transferred into glycogen
UDP
can glycogen synthase introduce new branches
no
can liver cells create free glucose from glycogen
yes
does glucagon inhibits glycogen synthesis and stimulate glycogen breakdown
yes
does insulin inhibit glycogen breakdown and stimulate glycogen synthesis
yes
is gluconeogensis a pathway for the synthesis of new glucose from non carbohydrate precursors
yes
true or false: lactate, glycerol and glucogenic amino acids are precursors for gluconeogensis
true
true or false: gluconeogensis is glycolysis run in reverse
false
does gluconeogenesis mainly occur in the liver
yes
is gluconeogenesis energy consuming
yes
does glucagon inhibit gluconeogensis
no it stimulates it
does insulin inhibit gluconeogenesis
yes
what do catabolic pathways do
break down substances for energy generation- uses reduced fuel to make oxidised products
what do anabolic pathways do
synthesise complex molecules out of smaller ones in energy-consuming reaction- uses oxidised precursors to make reduced biosynthetic products
what do anabolic pathways require
ATP for energy, reducing force in the from of NADPH
what do catabolic pathways generate
reduced cofactors which can drive oxidative phosphorylation
how many ATP does glycolysis produce per glucose thats broken down
2
what forms the first stage of carbohydrate catabolism
glycolysis
where does glycolysis occur
cytoplasm
how much NADH + H+ does glycolysis produce per glucose molecule
2
what are the three stages of glycolysis
1- glucose is trapped and destabilised
2- two interconvertible three carbon molecules
3- ATP generated
can pyruvate directly enter oxidative phosphorylation
no
what is pyruvate converted into that enters the TCA cycle
acetyl CoA
what does the TCA cycle provide precursors for
gluconeogenesis
breakdown products from what feed into the TCA cycle
carbohydrate, fat and protein metabolism
does the TCA cycle consume NADH and FADH2
no
where does the TCA cycle hapoen
in the mitochondrial matrix
briefly describe the TCA cycle
A two-carbon unit (from acetyl-CoA) condenses with a four-carbon unit
The resulting six-carbon unit is decarboxylated twice
-yields CO2
Four oxidation reactions
-yield NADH + H+ and FADH2
One GTP is formed
-energy
The four-carbon unit is recreated (to make the 6 carbon unit)
in oxidative phosphorylation what happens to NADH and FADH2
are tranferred onto oxygen
where is the electron transport chain located
in the inner mitochondria membrane
in oxidative phosphorylation where are protons pumped from and to
from mitochondrian matrix to intermembrane space
what direction is the proton conc gradient
from intermembrane space to mitochondrial matrix
what is proton flow coupled to
ATP synthesis
what systems does oxidative phosphorylation consist of
two separate proton pump systems
in oxidative phosphorylation what are electrons from NADH and FADH2 used to do
reduce O2 to H2O
energy from what pumps protons
electrons from NADH and FADH2
what does NADH donate electrons to
complex I
what does FADH2 donate electrons to
complex II
what complexes transport electrons alongside the pumping of H+
I, III and IV
what is the P/O ratio
a measure of the number of ATP molecules formed per oxygen atom reduced
what is the redox potential of a reduced molecule
its likelihood to loose an electron (in comparison with H2)
what does a more negative redox potential mean
it is more likely to loose an electron
how is the transfer of electrons linked to redox potential
Electrons can be transferred from molecules with negative redox potentials to those with more positive redox potentials
what does the difference in redox potential between substrate and product of a redox reaction relate to
the free energy change of the reaction
does NADH have a more positive or nagative redox potential than FADH2
more positive
what does a negative redox redox potential mean
the reduced form has a lower affinity for electrons that H2
what does a low redox potential mean (e.g. in oxygen)
that it is most likely to accept oxygen
what does transferring electrons from a negative to a positive redox potential do
releases energy
how is ATP formed from redox potentials
transferring electrons from a negative to a positive redox potential releases energy
Oxidative phosphorylation converts the energy inherent in these electrons into chemical energy in the form of ATP
