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BCH210H1 Study Guide - Glycerol Kinase, Acetyl-Coa, Mad2

Course Code
Michael Baker

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BCH210H © Lisa Zhao 2012 | Page 1
Lecture 33:
at 38 km
adrenaline is coursing through her blood
trying to get adrenaline up to mobilize more and more FFA that will take pressure off CHO
CHO is still being used
trying to avoid weakness in Krebs, hitting wall by gradually decreasing the use of glycogen at the
later stage of the race
P/O ratio NADH = 2.5
7 x 2.5 = 17.5 ATP
P/O ratio FADH2 = 1.5
7 x 1.5 = 10.5 ATP
in total, 28 ATP from the 7 cycles of β-oxidation
acetyl CoA goes on to Krebs in mitochondrial matrix
P:O is P:0.5O2
every time e- pair goes through ETC, 0.5O2 is used
whenever an ATP is made, an anhydride link is made from ADP to ATP, which generates a H2O
1 ATP = 1 H2O
thus, for every e- pair coming down from e- transport, a H2O is made
1 FAD = 1 H2O
10.5 + 7 = 17.5 H2O
1 NAD = 1 H2O
17.5 + 7 = 24.5 H2O
the one ATP formed by substrate-level phosphorylation in the auxillary rxn from Krebs does NOT
give H2O
high temps increase body temp
good that a lot of H2O is produced w β-oxidation of fat
as she is increasing fat percentage and lowering use of CHO, more and more H2O is produced
fat reserves provide a lot of water generation i.e. camels, whales
β-oxidation produces a lot of ATP AND H2O
the H2O rehydrates
the other problem is blood glucose
liver has limited amount of glycogen
athletes build up glycogen stores in muscle and liver
glycogen in liver is used to maintain blood sugar
glycogen levels are getting lower in muscle and liver
as she increases speed and relies on more and more fat, will she have enough glycogen to sustain
there is another way to make glucose
liver needs to sustain blood sugar to keep organs working
liver is resourceful
liver uses things in the blood
fat mobilization produces glycerol (major water component from triglyceride hydrolysis)
glycerol has 3C, needs 2 to make glucose
liver uses gluconeogenesis to use the glycerol (a lot of glycerol from fat mobilization)
BCH210H © Lisa Zhao 2012 | Page 2
can start from pyruvate lactate (recapture lactate that is produced)
but athletes don’t make a lot of lactate, so not a lot of pyruvate lactate made
pyruvate and lactate have 3C, so need 2 lactates
easier to make glucose from glycerol
glycerol kinase adds a P onto a OH on glycerol to produce glycerol phosphate
a DH changes an OH to a keto group, making dihydroxyacetone-P (DHAP)
dihydroxyacetone-P is one of the intermediates of glycolysis
some parts of glycolysis can be reversed
glycerol is in significant qualities in the blood
need 2 glycerols to make glucose
2 DHAPs produced
1 DHAP made into glyceraldehyde-3-P which combines with the other DHAP with aldolase
(favourable in reverse form, not favourable in glycolysis path) +26 in glycolytic direction, reverse is
-26, favourable
fru-1,6-bisP produced
there are other possible methods
from lactate (Pyruvate-lactate)
can’t reverse pyruvate kinase, so need detour
convert pyruvate to OAA
and all other rxns are reversible
can’t reverse PFK-1 (kinases are irreversible)
need another enzyme to convert fru-1,6-bisP to fru-6-P
f-1,6-bisphosphatase (FBP-1) found in liver
breaks off P-1
favourable rxn since it breaks off phosphate-ester
f-6-P isomerized to form g-6-p
can’t reverse hexokinase, but liver specific enzyme imp in glycogen breakdown, g6phosphatase to
produce glucose
glucose goes out into the blood using a transporter (since P is gone)
since less glucose in blood
but needs NRG
need either glycolysis dominant or gluconeogenesis dominant (shouldn’t have both)
they are reciprocally controlledthings that turn on one will turn off the other
ex. PFK-1 is stimulated by AMP and f-2,6-bisP in muscle, but inhibits FBP-1
activities associated w production and destruction of f-2,6-bisP are found in one enzyme
is an imp regulator in liver, so there are mechanisms to control it very precisely in liver
f-2,6-BP can be formedby PFK-2 and can be degraded by fru-2,6-bisphosphatase (FBP-2)
breaks ester at C-2
*FBP-1: gluconeogenesis, FBP-2: control of f2,6bp levels
one enzyme carries ability to make AND breakdown of f2,6bp
has 2 active sites
only one active site open at once
based on phosphorylation of the enzyme (covalent modification)
imp in endocrine regulation (at 38 km mark)
BCH210H © Lisa Zhao 2012 | Page 3
when glucagon binds (extreme catabolic mode), insulin low, adrenaline high, glycogen broken
down, triglycerides broken down
cAMP activates PKA which can turn off pyruvate kinase to slow liver glycolysis (slow liver’s use
of sugar), and at the same time PKA phosphorylates enzyme to turns off PFK-2 and turn on
bc don’t want glycolysis to be active in catabolism, want it to slow down a little
this promotes gluconeogenesis by getting rid of f-2,6bp which would inhibit it
to support blood sugar in the last km of the race
ATP supports gluconeogenesis