Lecture 32 Fat.docx

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Department
Biochemistry
Course
BCH210H1
Professor
Michael Baker
Semester
Fall

Description
BCH210H © Lisa | Page 12 Lecture 32: Fat  extreme running (after 2 hours) causes metabolic changes  has built-up glycogen reserves  lost considerable water  CHO = 4kcal of NRG  fat = 9kcal of NRG  At the 32 km mark she has used up 1000 kcal of energy: 175 g of glycogen and 33 g of fat  fat is a better fuel, but is organized in fat tissues and isn’t directly accessible to muscle, so signals must be sent to fat tissues to mobilize FFAs  already used 1/3 of glycogen and is using more and more fat to keep ATP levels  she is changing gears as she is mobilizing more and more fat  has to keep increasing the use of fat and not run out of glycogen  if glycogen reserves are gone, there is remarkable reduction in running efficiency  you “hit-the-wall”  Krebs has a weak point (the OAA)  OAA is used by citrate synthase  small formation of OAA, but rapid utilization, thus OAA levels are usually low  this will slow down Krebs unless you can support OAA  OAA can be supported by MDH, but the rxn is not that favourable  there is another way to make OAA  use pyruvate to make OAA  pyruvate is from CHO, thus need glycogen  any small level of pyruvate can support OAA levels  she is under a lot of heat and intense exercise  glycogen is easily mobilized but fat takes time  glucagon increases  liver is supporting blood sugar  liver using glycogen to produce glucose  liver wants to suppress glycolysis to save glucose for other tissues  cuts down its own glycolytic rate  PKA is up with adrenaline and glucagon  PKA phosphorylates pyruvate kinase and slow down glycolysis  also slows down PFK-2 (which makes the allosterically strong allosteric activator in liver—fru- 2,6-bisP)  shuts down production of fru-2,6-bisP  liver shuts down glycolysis and tries to bring in fat as its principle NRG source  liver has fixed NRG need, but muscle has more and more requirements during exercise  slowing of glycolysis results in beta-oxidation, giving more ATP—liver response to get its rate down  glycolysis low in liver to preserve glucose for blood and brain  now need to draw on fat  training increases ability to change gears from glycogen to fat use  muscle is different from liver, doesn’t make sacrifice, doesn’t stop glycolysis  need glycolysis to support OAA levels to pyruvate  has both glycolysis and beta-oxidation working  muscle increases fat use to provide ATP (beta-oxidaiton) and diminish glycogen BCH210H © Lisa| Page 212 Fat Cells  after prolonged exercise, fat cells will response and be used  most reserves are in the form of fat bc fat can be stored in an anhydrous, with no water involved  droplets of oil organized in the cellular structure  fat cells have adrenaline receptors and glucagon receptors o exercising as well as fasting draws fat o fasting draws fat bc glucagon triggers the receptor and results in a signalling response  receptor → G-proteins  GTP cativates adenylate cyclise which activates ATP and cAMP turns on PKA (same as for glycogen)  (different) if drink coffee on empty stomach, it increases efficiency bc caffeine inhibits breakdown of cAMP (and also increase adrenaline release)  sustains cAMP, thus allowing PKA to be active for a longer period of time  PKA has diff targets in fat cells  phosphorylates HSL (is an esterase like LipoProtein Lipase that breaks triglycerides)  HSL hydrolyzes TGL, breaking the ester links at 1 and 3 positions  another enzyme, monoglyceride lipase, gets fatty acid off of bidyl (at C-2 of glycerol)  thus, need combination of HSL and MGL to ultimately give 3 FFA and glycerol  another enzyme, adipocyte triglyceride lipase (ATGL) used to support breakdown of triglyceride (not turned on by phosphorylation) o attacks central oil droplet in fat cell resulting in hydrolysis and FFA and glycerol release  FFA comes out and gets bound to albumin o takes it around body o albumin circulates it  caffeine prolongs effect of cAMP and thus prolongs affect of adrenaline and thus breaks down FFA w increasing speed and efficiency as more and more adrenaline and more and more PKA and these effects are sustained  she also engages in singing in her mind to increase adrenaline release  FFA produced FFA Activation  need
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