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154 Cards in this Set

  • Front
  • Back
Energy STORAGE
Anabolic/Building
Energy MOBILIZATION
Catabolic/Breaking Down
Besides storage & Mobilization what is the 3rd main direction of metabolism? (Dep on fuel avail)
Conversions
fuel stores are interconnected thru
spinal column of C compounds by a MULT of pathways
Direction of Pathways are controlled by (give 4)
1.Horm
2.Nervous System
3.ATP/ADP ratios
4.accum of intermed/endproducts
what det cat/ana
Hormones
main hormones
insulin & glucagon
Emergency hormones
cortisol & epinephrine
Back up hormones
Thyroid & Growth Hormone
Explain how we get gluc
-glucose from food
-if cant, then glycogen from LIVER
-if cant, make new via GlucoNEOgenisi
synthesis of new glucose from precursors=
glucoNEOgenisis
Storing Glucose=
Glyco-genesis
releasing stored glucose=
*think "L" letting Loose that stored up glucose!!...2L's
gLycogenoLysis
Gluc-Dep tissues..
*remember..
Nervous,RRR,hands down...
Nerv System
Retins, RBC's, Renal Med
gonads, Fetus, lactation
main level of Gluc=
80-120 mg Glc/dl
below 80 =
irratibility.<80=seizures
<50=
coma
<20=
death
preferred order of what body will burn for energy=
glucose..if non..then fat..then protein
Hyper=
Norm=
Hypo=
Hyper >120
Norm 80-120
Hypo<80
what 3 hormones respond by (INC in blood gluc)=
1.Glucagon
2. Cortisol
3. Norepinephrine
What responds when (careful here..) blood glucose is increased?
insulin increases
What can reverse in glucose trapping?
(irreversible everywhere else..)
when we say reversable we mean these tissues can "give back" blood glucose after it goes into the cell.
-Liver
-Kidneys
-GI cells
can all reverse blood glucose
main organ contributing to glucose homeostasis=
liver
most tissues hurry and ....do what to Gluc
Phosphorylize to Gluc-6-P--->now can diffuse back out
is Liver glucose dependent?
NO (it does have perm GLUTS in membrane though) thats why we say Gluc-Dep + Liver......
fac Diff only when
insulin present
Fate of energy
Gain(Catabolic)
Storage (anabolic)
tell me the 2 ways energy can be gained:
Anaerobic
Aerobic
Aerobic Conditions:
glycoloysis-AcetylCoA-Krebs-ETC
(in the Aer we get glycoloysis(same in both...and here we get Ace&Kreb ETC..)
Anaerobic Conditions:
Glycolysis -lactic Acid/lactate formation

(lay around and not exercise you get Glycolysis (same in both) but here you get lactic acid)
Energy Storage=
Anabolic
1. Glycogen
2. Conversion of Glc into Fatty Acids
3.Protein Pool
are Anabolic and Catabolic on at same time?
yes
Fac Diff needs 2 things:
1. transporter(big channel type protein) GLUTS
2. Concentration gradient
...then glucose can diff
hypoglycemia means we need=
Glucagon
Cortisol or
Norepinephrine
Hyperglycemia
Insulin
Hyperglycemia ex she gave
D. Mellitis-inc osmolality-water influx
Insulin does what
puts away blood glucose
and
stim tiss to use it
sorry to through this in from 2nd page but i dont want her to ask us and us not know..
C6=
hexose
C3=
Pyruvate & glycerol
C2 =
Acetyl Group
C1=
Carbon Dioxide
Glycolysis/Catabolic/Aerobic Conditions....so where does Glycolysis take place?
Cytoplasm
Glycolysis(cytoplasm)=?=?

fyi..think the enzymes for glycolysis are all in the cytoplasm
splitting of C6 into 2(C3's)
=pyruvates
point of glycolysis is (explain "splitting" reason...next question we'll explain the other purposes..)
to split glucose molecule from 6 carbons into 2 pyruvates 3 carbons each...pyruvates can fit into mitochondria
purpose of glycolysis
ok yatta yatta (we know to split..)
-ATP is generated (2) per gluc
-NADH2...(glucose' chem energy is transferred/stored via Hydrogen in the form of NADH/H+ for entry into the ETC!!)
what is NADH2
glucose' chem energy is transferred/stored via Hydrogen in the form of NADH/H+ for entry into the ETC
What enter Mitocondria?
pyruvate C3
after Pyruvate enter Mito ...
is Decarboxylated to Acetyl Group
=C2
after C3 goes to C2 (de-carn-oxylated to acetyl group) C2 does what!
hooks up with Coenzyme A (=AcetylCoA)
Once we have Acetyl CoA..
Ready to enter Kreb Cycle baby!!
so again... why do we need aerobic/glycolysis pathway!
(give 2 reasons)
-prod ATP (2 per gluc)
-prod some reduce Co Factor:NADH2
(and yes that's what she said..reduce CoFactor...whatever she's German..)
Why is NADH2 always important
b/c it takes over the energy rich HYDROGEN ions from the incoming substrate
Why is NADH2 always important
-energy is contained in their bond
-in the end the energy goes to ETC
Why is NADH2 always important
(one more time..tell me)
this is a carrier for Chem Energy to transport this energy later to the ETC!!

-We need glycolysis in order to CATabolize gluc totally in the Krebs cycle and ETC and unless it's made smaller it wont fit in the Mitocondria so..split into pyruvate and waalaa into Mito (& we get ATP and energy tran to the H & ready for ETC)
Whats the next step after Glycolytic Pathway
Enter in Mitocondria
What happens whe we come into the Mito-con-dria!!
loose a Carbon becomes C2
now that we're inside the Mitocondria and we've paid up by give a Carbon away..what happens?
now we just have a run of the mill Acetyl group C2...and it immediately wants a date so it hooks up with co-facto--Co-enzyme A
(=Acetyl CoA)
Acetyl CoA is ready for??
KREBS CYCLE
Urine pH and drug elimination

Trapped in acidic environments.
Weak bases

Thus treat OD with a strong acid to trap them in the tubules = ammonium chloride
Would you say Kreb Cycle produces energy?
No
so Acetyl CoA enters Kreb Cycle and what happens
you got it...once again
DE-CARB-oxylation AND also De-hydration....)
So Kreb Cycle is basically
series of enzymatic degredations
1.De-Carb-oxylation
2.De-hydration
Explain what happens from entrance of the AcetylCoA into Krebs..
Carbons fly off (waste)
*chem energy trans to more co-factores=NAD & NADH2
how many ATPs does Kreb make?
1 ATP
Kreb Cycle is where
Mitocondria
Kreb Cycle =
2 CO2
1ATP
8 Hydrogens atoms (NADH/H+)
What does AcetylCoA hook up with in the Krebs?
OAA (C4)
so OAA(C4) +(C2 the acetyl CoA)=
CITRIC ACID

C4+C2=Citric Acid C6
then what happens to C6
De-Carb-oxylations and dehydrations ending again in OAA
Kreb Cycle starts and ends with?
OAA
most important outcome of glucose oxidation in the Krebs Cycle is making______?
making the ENERGY RICH hydrogen ions avail for future oxidation in the ETC!!!!!!!!!
What are some additional jobs of the Kreb :)
synth Fat ass & AA
synth gluc
synth comBUSTion of fat ass & AA
(Kreb is a busy dude...)
what the "stored" energy that we're gonna use for ETC?
NADH/H+
Why is NADH2 always important( or aka NADH/H+) ??
NADH2 is transferred to ATP=Oxidative Phosphorylation
ETC=
series of electron carriers integrated into the INNER mitochondrial membrane.....energy stored NADH2 is transferred to ATP=oxidat phosph
the Oxi Pho leads to (3) important things
-gen of ATp
-regeneration of NAD
-formation of water out of the remaining protons & oxygen
What goes in ETC?
NADH2
what comes out ETC?
-ATP=energy carrier*
-NAD=regenerated
-Water
**MUST HAVE OXY or cant use ETC**
What if no oxygen is avail for ETC?
NADH2 will pile up
What if NADH2 piles up? What consequence on Kreb cycle?
Kreb can't work without NAD
If we dont regenerate NAD can NADH2 thats avail make Kreb work?
Nope
=inhibition
What if Kreb doesnt run?
Acetyl CoA piles up
If Kreb Cycle stops and Acetyl CoA piles up then....
pyruvate can't be converted to Acetyl
If pyruvate piles up....
Glycolytic pathway stops
(-ATP production would cease totally)
Prod accumulation @ end of a reaction (when no co-factor avail) .....
a reaction will come to a stand still
this situation is what we call?
Anaerobic situation (lack of oxygen)
what can cause lack of oxy?
-decreased Circulation
-Ischemic (maybe mini stroke)
-compression of vessels
-increase sympath tone (inc HR,dec dig,contracting blood vess)
-EXERCISE
-Generalized anemia
So what needs to happen to keep glycolysis OPEN for business?
-Pyruvate must be removed
-NAD regenerated via LACTATE
Pyruvate is reduced to lactic Acid by?
LDH (lactate dehydrogenase hormone)
Pyruvate is reduced to lactic acid by LDH this generates?
NAD ( so now some ATP can still be generated via glycogenolysis)
What is the main energy pathway for RBC's?
Anaerobic (b/c they have no Mitocondria)
so now we got Lactic Acid...what now?
need to get rid of it..certain places like heart & liver..can help us out with getting rid of it b/c they rarely run out of O2..)
LDH converts?
Pyruvate to Lactic Acid

AND

Lactic Acid back to Pyruvate
pyruvate + H2 =
(with LDH help)
Lactic acid
once lactic acid is changed back to pyruvate (thanks to LDH) what do we see?
aerobic pathway-back to Krebs--ETC-enters glucoNEOgenisis in liver to produce new glucose
what do heart and liver do to help keep us from building up lactic acid ...
they help get lactate back on aerobic track--> pyruvate-> Krebs-> ETC
LDH converts
lactate to pyruvate
-found where we have anaerobic
-found in Skelatal Musc
-RBS
-Liver,GI,Kidney
-theoretically not in Plasma but LDH can mean tiss damage
LDH
converts lactate back to Pyruvate
LDH
should only be found in small amount in plasma
LDH found where?
Muscle
liver
RBC
GI tract
kideys
(and if there is tissue damage-inplasma..little is normal..)
excess glucose stored as
glycogen in Liver and muscle
(use later for glucogenesis)
is glycogen osmotically active?
no
main glycogen storing organs are
Liver-6% max of own weight
muscle-1% max
when small gluc-chains form in alpha 1-4 linkages....
Branching Enzyme transferes groups of 6 glc units as side chains in alpha 1-6 linkages =branched carbohydrate
in glucose is needed for energy
glycogen broken down to Glc-6-P= Glycogenolysis
glycogenolysis requires
de-branching enzyme
for Glc-6-phosphate to get into circ we need
Phosphatase
Is phosphatase found in muscle cells?
NO, only hepatic glycogenolysis can increase blood glucose levels
Muscle glycogenolysis
increases Muscle energy supply
blood glucose low & glycogen stores empty=
glucose synthesized to supply Gluc-Dep tissues=GLUCO-NEO-GENISIS (liver & Kid)
Gluco-neo precursors are
many AA
lactate
Propionate out of Fermentation
Glycerol from triglyceride breakdown
Precursor enter Krebs and are..
pulled out of cytoplasm as OAA/Malate

-to enter gluconeo (except glycerol)
Both ____ & ____ contain phosphatase & release free glucose into circulation
Liver & Kid
Lipids are
hydrophobic (must be made soluble for transport in plasm by combining with PROTEINS
what are lipoproteins
lipids surrounded by a shell of hydro-philic proteins & phospholipids and specific recepto proteins=APOProteins
VIP receptor protein=
Apoproteins
2 classes of lipoproteins
-chylomicron
-VLDL
Chylomicrons are
formed by small intestinal ENTEROcytes AFTER absorption of lipids
VLDL are formed...
by LIVER cells
-after PRODUCTION of new lipids
Chylo/VLDL circulate and then..
their Apoproteins bind to endo rec & act endo LPL's
LPL's do what
dissolve shell & hydrolyze triglycerides
once shell dissolves and triglycerides are hydrolized....
FREE fatty acids + glycerol diffuse into respective tiss for STORAGE & ENERGY
After diffusion into Adi-po-cytes, what do triglycerides do?
Reform=fat storage form
Release of stored fat=
Lipolysis
how is lipolysis initiated?
when circulating fuel levels (glc) are LOW & energy is needed
HSL hydrolyzes
(Hey See ya Later FFA & Gly)
triglycerides to FFA's and glycerol BACK into circulation
FFA's bind to?
plasma Albumin for transport
(they Al BUM a ride)=NEFA
NEFA's deliver
FFA's to Active tissues for energy GAIN
FFA's can originate from
NEFA's
VLDL's
Chylomicrons
After cell entry FFA's
enter mitocondria & undergo progressive release of C2 segments
these C2 segments are
Acetyl CoA=BETA oxidation
Acetyl CoA enters Krebs for
complete oxidation &
ATP generation in the ETC
FFa's are utilized for energy GAIN by
entering BETA-oxidation
Beta-Oxidation releases
Acetyl groups for use in Krebs cycle/ETC
What diffuses into active tissues
Glycerol
Glycerol can
enter glycolysis->Krebs->ETC when ATP is needed
OR Glycerol can
enter Gluco-NEO-genisis when glucose is needed
Excess glucose & AA can be converted into FFA's =
Lipo-genisis
Lipogenisis happen in
Liver
Fat Tissue
Mammary Gland
What activates Lipo-genesis?
when stores of ATP, Glycogen & Labile Protein are FULL & Glc & AA are still avail
FFA's are ______ into ____for storage
condensed into TG's for storage
(adipocytes only) or secreted in milk
is Liver a fat storage site?
NO
Liver packs newly produced TG's into
Lipoproteins=VLDL's
Lipoproteins=VLDL's--->
Exo-cytosis into circulation
Exo-cytosis into circulation----> Fat Tissue LPL's ______
(bringing the fat in)
hydrolyze VLDL's--->fat storage
During Lipolytic phases the Liver
readily takes up FFA's from NEFA's without using them for energy
=acts like a FAT SPONGE
Liver basically pawns the fat off to other tissues (or makes it availible however you want to see it) but it gives it them out as (2 types)
1. VLDL's
2.Ketone Bodies
liver sponges up FFA's and NEFA's and gives out
VLDL's & KB
Ketone Bodies=
accumulation Acetyl groups condense into Acetoacetic Acid & Beta-HydroxyButyrate
KB formation
irreversible, release into blood, other tissues take them up,
after other tiss take up KB...
they get changed back into Acetyl CoA-->enter KREBS/ETC for energy GAIN
Liver Beta-oxidizes FFA for other tissues & supplies an easily ...
usable hydroPHILic substance for energy gain (for example Neurons & muscles)
KB are
Physiological and VIP energy source for many tissues when glucose levels are LOW.