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154 Cards in this Set
- Front
- Back
Energy STORAGE
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Anabolic/Building
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Energy MOBILIZATION
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Catabolic/Breaking Down
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Besides storage & Mobilization what is the 3rd main direction of metabolism? (Dep on fuel avail)
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Conversions
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fuel stores are interconnected thru
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spinal column of C compounds by a MULT of pathways
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Direction of Pathways are controlled by (give 4)
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1.Horm
2.Nervous System 3.ATP/ADP ratios 4.accum of intermed/endproducts |
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what det cat/ana
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Hormones
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main hormones
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insulin & glucagon
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Emergency hormones
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cortisol & epinephrine
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Back up hormones
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Thyroid & Growth Hormone
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Explain how we get gluc
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-glucose from food
-if cant, then glycogen from LIVER -if cant, make new via GlucoNEOgenisi |
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synthesis of new glucose from precursors=
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glucoNEOgenisis
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Storing Glucose=
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Glyco-genesis
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releasing stored glucose=
*think "L" letting Loose that stored up glucose!!...2L's |
gLycogenoLysis
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Gluc-Dep tissues..
*remember.. Nervous,RRR,hands down... |
Nerv System
Retins, RBC's, Renal Med gonads, Fetus, lactation |
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main level of Gluc=
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80-120 mg Glc/dl
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below 80 =
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irratibility.<80=seizures
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<50=
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coma
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<20=
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death
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preferred order of what body will burn for energy=
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glucose..if non..then fat..then protein
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Hyper=
Norm= Hypo= |
Hyper >120
Norm 80-120 Hypo<80 |
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what 3 hormones respond by (INC in blood gluc)=
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1.Glucagon
2. Cortisol 3. Norepinephrine |
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What responds when (careful here..) blood glucose is increased?
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insulin increases
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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 |
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main organ contributing to glucose homeostasis=
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liver
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most tissues hurry and ....do what to Gluc
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Phosphorylize to Gluc-6-P--->now can diffuse back out
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is Liver glucose dependent?
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NO (it does have perm GLUTS in membrane though) thats why we say Gluc-Dep + Liver......
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fac Diff only when
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insulin present
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Fate of energy
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Gain(Catabolic)
Storage (anabolic) |
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tell me the 2 ways energy can be gained:
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Anaerobic
Aerobic |
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Aerobic Conditions:
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glycoloysis-AcetylCoA-Krebs-ETC
(in the Aer we get glycoloysis(same in both...and here we get Ace&Kreb ETC..) |
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Anaerobic Conditions:
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Glycolysis -lactic Acid/lactate formation
(lay around and not exercise you get Glycolysis (same in both) but here you get lactic acid) |
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Energy Storage=
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Anabolic
1. Glycogen 2. Conversion of Glc into Fatty Acids 3.Protein Pool |
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are Anabolic and Catabolic on at same time?
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yes
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Fac Diff needs 2 things:
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1. transporter(big channel type protein) GLUTS
2. Concentration gradient ...then glucose can diff |
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hypoglycemia means we need=
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Glucagon
Cortisol or Norepinephrine |
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Hyperglycemia
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Insulin
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Hyperglycemia ex she gave
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D. Mellitis-inc osmolality-water influx
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Insulin does what
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puts away blood glucose
and stim tiss to use it |
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sorry to through this in from 2nd page but i dont want her to ask us and us not know..
C6= |
hexose
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C3=
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Pyruvate & glycerol
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C2 =
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Acetyl Group
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C1=
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Carbon Dioxide
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Glycolysis/Catabolic/Aerobic Conditions....so where does Glycolysis take place?
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Cytoplasm
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Glycolysis(cytoplasm)=?=?
fyi..think the enzymes for glycolysis are all in the cytoplasm |
splitting of C6 into 2(C3's)
=pyruvates |
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point of glycolysis is (explain "splitting" reason...next question we'll explain the other purposes..)
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to split glucose molecule from 6 carbons into 2 pyruvates 3 carbons each...pyruvates can fit into mitochondria
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purpose of glycolysis
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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!!) |
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what is NADH2
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glucose' chem energy is transferred/stored via Hydrogen in the form of NADH/H+ for entry into the ETC
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What enter Mitocondria?
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pyruvate C3
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after Pyruvate enter Mito ...
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is Decarboxylated to Acetyl Group
=C2 |
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after C3 goes to C2 (de-carn-oxylated to acetyl group) C2 does what!
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hooks up with Coenzyme A (=AcetylCoA)
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Once we have Acetyl CoA..
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Ready to enter Kreb Cycle baby!!
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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..) |
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Why is NADH2 always important
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b/c it takes over the energy rich HYDROGEN ions from the incoming substrate
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Why is NADH2 always important
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-energy is contained in their bond
-in the end the energy goes to ETC |
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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) |
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Whats the next step after Glycolytic Pathway
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Enter in Mitocondria
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What happens whe we come into the Mito-con-dria!!
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loose a Carbon becomes C2
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now that we're inside the Mitocondria and we've paid up by give a Carbon away..what happens?
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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) |
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Acetyl CoA is ready for??
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KREBS CYCLE
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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 |
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Would you say Kreb Cycle produces energy?
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No
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so Acetyl CoA enters Kreb Cycle and what happens
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you got it...once again
DE-CARB-oxylation AND also De-hydration....) |
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So Kreb Cycle is basically
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series of enzymatic degredations
1.De-Carb-oxylation 2.De-hydration |
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Explain what happens from entrance of the AcetylCoA into Krebs..
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Carbons fly off (waste)
*chem energy trans to more co-factores=NAD & NADH2 |
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how many ATPs does Kreb make?
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1 ATP
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Kreb Cycle is where
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Mitocondria
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Kreb Cycle =
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2 CO2
1ATP 8 Hydrogens atoms (NADH/H+) |
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What does AcetylCoA hook up with in the Krebs?
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OAA (C4)
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so OAA(C4) +(C2 the acetyl CoA)=
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CITRIC ACID
C4+C2=Citric Acid C6 |
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then what happens to C6
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De-Carb-oxylations and dehydrations ending again in OAA
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Kreb Cycle starts and ends with?
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OAA
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most important outcome of glucose oxidation in the Krebs Cycle is making______?
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making the ENERGY RICH hydrogen ions avail for future oxidation in the ETC!!!!!!!!!
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What are some additional jobs of the Kreb :)
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synth Fat ass & AA
synth gluc synth comBUSTion of fat ass & AA (Kreb is a busy dude...) |
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what the "stored" energy that we're gonna use for ETC?
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NADH/H+
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Why is NADH2 always important( or aka NADH/H+) ??
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NADH2 is transferred to ATP=Oxidative Phosphorylation
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ETC=
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series of electron carriers integrated into the INNER mitochondrial membrane.....energy stored NADH2 is transferred to ATP=oxidat phosph
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the Oxi Pho leads to (3) important things
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-gen of ATp
-regeneration of NAD -formation of water out of the remaining protons & oxygen |
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What goes in ETC?
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NADH2
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what comes out ETC?
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-ATP=energy carrier*
-NAD=regenerated -Water **MUST HAVE OXY or cant use ETC** |
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What if no oxygen is avail for ETC?
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NADH2 will pile up
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What if NADH2 piles up? What consequence on Kreb cycle?
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Kreb can't work without NAD
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If we dont regenerate NAD can NADH2 thats avail make Kreb work?
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Nope
=inhibition |
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What if Kreb doesnt run?
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Acetyl CoA piles up
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If Kreb Cycle stops and Acetyl CoA piles up then....
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pyruvate can't be converted to Acetyl
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If pyruvate piles up....
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Glycolytic pathway stops
(-ATP production would cease totally) |
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Prod accumulation @ end of a reaction (when no co-factor avail) .....
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a reaction will come to a stand still
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this situation is what we call?
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Anaerobic situation (lack of oxygen)
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what can cause lack of oxy?
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-decreased Circulation
-Ischemic (maybe mini stroke) -compression of vessels -increase sympath tone (inc HR,dec dig,contracting blood vess) -EXERCISE -Generalized anemia |
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So what needs to happen to keep glycolysis OPEN for business?
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-Pyruvate must be removed
-NAD regenerated via LACTATE |
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Pyruvate is reduced to lactic Acid by?
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LDH (lactate dehydrogenase hormone)
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Pyruvate is reduced to lactic acid by LDH this generates?
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NAD ( so now some ATP can still be generated via glycogenolysis)
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What is the main energy pathway for RBC's?
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Anaerobic (b/c they have no Mitocondria)
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so now we got Lactic Acid...what now?
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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..)
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LDH converts?
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Pyruvate to Lactic Acid
AND Lactic Acid back to Pyruvate |
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pyruvate + H2 =
(with LDH help) |
Lactic acid
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once lactic acid is changed back to pyruvate (thanks to LDH) what do we see?
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aerobic pathway-back to Krebs--ETC-enters glucoNEOgenisis in liver to produce new glucose
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what do heart and liver do to help keep us from building up lactic acid ...
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they help get lactate back on aerobic track--> pyruvate-> Krebs-> ETC
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LDH converts
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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 |
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LDH
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converts lactate back to Pyruvate
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LDH
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should only be found in small amount in plasma
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LDH found where?
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Muscle
liver RBC GI tract kideys (and if there is tissue damage-inplasma..little is normal..) |
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excess glucose stored as
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glycogen in Liver and muscle
(use later for glucogenesis) |
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is glycogen osmotically active?
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no
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main glycogen storing organs are
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Liver-6% max of own weight
muscle-1% max |
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when small gluc-chains form in alpha 1-4 linkages....
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Branching Enzyme transferes groups of 6 glc units as side chains in alpha 1-6 linkages =branched carbohydrate
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in glucose is needed for energy
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glycogen broken down to Glc-6-P= Glycogenolysis
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glycogenolysis requires
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de-branching enzyme
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for Glc-6-phosphate to get into circ we need
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Phosphatase
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Is phosphatase found in muscle cells?
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NO, only hepatic glycogenolysis can increase blood glucose levels
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Muscle glycogenolysis
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increases Muscle energy supply
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blood glucose low & glycogen stores empty=
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glucose synthesized to supply Gluc-Dep tissues=GLUCO-NEO-GENISIS (liver & Kid)
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Gluco-neo precursors are
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many AA
lactate Propionate out of Fermentation Glycerol from triglyceride breakdown |
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Precursor enter Krebs and are..
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pulled out of cytoplasm as OAA/Malate
-to enter gluconeo (except glycerol) |
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Both ____ & ____ contain phosphatase & release free glucose into circulation
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Liver & Kid
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Lipids are
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hydrophobic (must be made soluble for transport in plasm by combining with PROTEINS
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what are lipoproteins
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lipids surrounded by a shell of hydro-philic proteins & phospholipids and specific recepto proteins=APOProteins
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VIP receptor protein=
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Apoproteins
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2 classes of lipoproteins
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-chylomicron
-VLDL |
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Chylomicrons are
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formed by small intestinal ENTEROcytes AFTER absorption of lipids
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VLDL are formed...
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by LIVER cells
-after PRODUCTION of new lipids |
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Chylo/VLDL circulate and then..
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their Apoproteins bind to endo rec & act endo LPL's
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LPL's do what
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dissolve shell & hydrolyze triglycerides
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once shell dissolves and triglycerides are hydrolized....
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FREE fatty acids + glycerol diffuse into respective tiss for STORAGE & ENERGY
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After diffusion into Adi-po-cytes, what do triglycerides do?
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Reform=fat storage form
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Release of stored fat=
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Lipolysis
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how is lipolysis initiated?
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when circulating fuel levels (glc) are LOW & energy is needed
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HSL hydrolyzes
(Hey See ya Later FFA & Gly) |
triglycerides to FFA's and glycerol BACK into circulation
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FFA's bind to?
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plasma Albumin for transport
(they Al BUM a ride)=NEFA |
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NEFA's deliver
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FFA's to Active tissues for energy GAIN
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FFA's can originate from
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NEFA's
VLDL's Chylomicrons |
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After cell entry FFA's
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enter mitocondria & undergo progressive release of C2 segments
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these C2 segments are
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Acetyl CoA=BETA oxidation
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Acetyl CoA enters Krebs for
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complete oxidation &
ATP generation in the ETC |
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FFa's are utilized for energy GAIN by
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entering BETA-oxidation
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Beta-Oxidation releases
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Acetyl groups for use in Krebs cycle/ETC
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What diffuses into active tissues
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Glycerol
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Glycerol can
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enter glycolysis->Krebs->ETC when ATP is needed
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OR Glycerol can
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enter Gluco-NEO-genisis when glucose is needed
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Excess glucose & AA can be converted into FFA's =
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Lipo-genisis
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Lipogenisis happen in
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Liver
Fat Tissue Mammary Gland |
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What activates Lipo-genesis?
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when stores of ATP, Glycogen & Labile Protein are FULL & Glc & AA are still avail
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FFA's are ______ into ____for storage
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condensed into TG's for storage
(adipocytes only) or secreted in milk |
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is Liver a fat storage site?
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NO
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Liver packs newly produced TG's into
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Lipoproteins=VLDL's
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Lipoproteins=VLDL's--->
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Exo-cytosis into circulation
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Exo-cytosis into circulation----> Fat Tissue LPL's ______
(bringing the fat in) |
hydrolyze VLDL's--->fat storage
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During Lipolytic phases the Liver
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readily takes up FFA's from NEFA's without using them for energy
=acts like a FAT SPONGE |
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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)
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1. VLDL's
2.Ketone Bodies |
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liver sponges up FFA's and NEFA's and gives out
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VLDL's & KB
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Ketone Bodies=
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accumulation Acetyl groups condense into Acetoacetic Acid & Beta-HydroxyButyrate
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KB formation
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irreversible, release into blood, other tissues take them up,
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after other tiss take up KB...
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they get changed back into Acetyl CoA-->enter KREBS/ETC for energy GAIN
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Liver Beta-oxidizes FFA for other tissues & supplies an easily ...
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usable hydroPHILic substance for energy gain (for example Neurons & muscles)
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KB are
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Physiological and VIP energy source for many tissues when glucose levels are LOW.
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