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An in-depth exploration of digestive enzymes, their locations in the gi tract, and mechanisms of absorption. It also covers the comparison and contrast of insulin and glucagon activities on different tissues during fed and fasting metabolism. Additionally, it discusses the pathologies of diabetes mellitus type 1 and type 2.
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1.1.2.2.3.3. 4.4.5.5.^ Metabolic EnergyMetabolic Energy Reactants: glucose, Glycogen,Reactants: glucose, Glycogen,FasFas, Amino acidsPhosphorylationPhosphorylationGlycolysisGlycolysis –Citric Acid Cycle (Krebs, TCA)Citric Acid Cycle (Krebs, TCA) ÆÆ Electron Transport system (ETC)Electron Transport system (ETC) • • • • • • 2 ATPs2 ATPs, Amino acids2 ATPs,2 ATPs, anaerobicmitochondria,mitochondria, aerobicHigh energyHigh energyProduction:Production:OverviewOverviewReview &Review &– cytoplasmanaerobiccytoplasm ee-- aerobic (^) ÆÆ ≈≈ 32 ATPs32 ATPs Figure 22Figure 22--3: Summary of biochemical pathways for energy production3: Summary of biochemical pathways for energy production 1.1. Reversible Metabolism:Metabolism: Anabolic 222 2. Carbohydrates3.3. Amino Acids .Reversiblepathways shift topathways shift to pathwayspathways shift to anabolicanabolic CarbohydratesCarbohydratesCarbohydratesenergize synthesisenergize synthesis& storage& storageAmino Acids builtinto proteins,into proteins,surplus storedsurplus stored – – – –^ A. “A. “Fed State Different enzyme systemsDifferent enzyme systemsregulate the direction ofregulate the direction ofmetabolismmetabolismDefyDefy equ’mequ’m as necessary! Fed State” or (^) processesprocesses as necessary! shift tobuilt Anabolic ProcessesFigure 22Figure 22-” or Absorptive-4: 4 Dual (4: 4 Dual (Absorptive pushpush- Processes -pullpull ) control of metabolism) control of metabolism
1.1. In adipose cells2.2. In blood: 333 3. Conversion in liver4.4. Excreted in 5.5. Used for energy &. In adipose cellsIn blood: Conversion in liverConversion in liverConversion in liverExcreted in bile(excess)(excess) Used for energy &synthesissynthesis – – – – – – FAs, cholesterol–– (plaque build up) Long Term Nutrient StorageLong Term Nutrient StorageHDLHDL ((more LDLLDL FAs, cholesterol(plaque build up)more protprot/ (less(less prot/^ B.B. apoAapoA (& E) prot/ Figure 22Figure 22-and fate of dietary fatsand fate of dietary fats/^ (& E)apoBapoB bileFat Metabolism:Fat Metabolism: )) (^) -5: TransportÆÆÆÆ5: Transport bodybody)liverliver),),) RecRec-endocytosisendocytosis ExocytosisExocytosis LymphaticLymphatictransporttransport-med’dmed’d ÆÆ lipaseslipases TGTG TGTG FFAFFA
Dominates inDominates in Fed State^ CATABOLISMCATABOLISMfor releasefor releaseRegulate MetabolismRegulate MetabolismA.A. Insulin^ Insulin & GlucagonInsulin & GlucagonInsulin Action on Cells:Fed State MetabolismANABOLISMANABOLISMANABOLISMANABOLISMfollowing uptakefollowing uptakeAction on Cells:controlled by insulin and glucagoncontrolled by insulin and glucagonMetabolism^ = RATIO, not absolute= RATIO, not absoluteconcentrations, thatconcentrations, that^ Figure 22Figure 22-regulates!!regulates!!^ regulates!!regulates!!-9: Metabolism is9: Metabolism is
2. Insulin Effects: Resting Skel2. Insulin Effects: Resting Skel^ 1. Insulin Action1. Insulin Action --Musc & Adipose vs. Liver:Musc & Adipose vs. Liver:^ Figure 22Figure 22--11: Insulin’s cellular mechanism of action-- Fed State11: Insulin’s cellular mechanism of actionFed State Resting Skel Musc/ Adipose:Resting Skel Musc/ Adipose:Figure 22Figure 22- • • • • • • ** GLUT4GLUT4 removed when insulinremoved when insulingonegone only take** only take-** do not secrete!** do not secrete!** **exercising muscleexercising muscle Inserted automatically inInserted automatically in -12^12 inserted re: insulin,inserted re: insulin,-up glucose;up glucose; ((↑↑CaCa++++,, ↓↓Pi)Pi) ,, Liver:Liver:present!!present!! Directiontransport reg’d by gluctransport reg’d by glucequilibriumequilibrium^ GLUT2GLUT2 g6pg6pDirection of ≠≠ glc!!glc!!^ alwaysalways ofFigure 22Figure 22--13 13
22.5)22.5) Diabetes Mellitus^ GlucagonGlucagon ActionAbnormally Elevated BloodAbnormally Elevated Blood^ Figure 22-15: Endocrine response to hypoglycemiaDiabetes Mellitus:Action ---- FastingFasting State^ GlGl^ GlGlucagon:^ PREVENTSPREVENTSHYPOHYPOGLYCEMIA! ucagon: GLYCEMIA! State:
MellitusMellitus- FiFiFigFigure 22-AcuteAcutepathophysiology ofpathophysiology of type 1 diabetestype 1 diabetesmellitus (insulinmellitus (insulindeficiency)deficiency)^ DiabetesDiabetes glycemia)glycemia) (Hyper(Hyper- ure 22 2222 -16: 1616 16: - -I:I: H+/K+ ATPaseH+/K+ ATPaseantiporterantiporter VasopressinVasopressin 1.1. Over 15 million diabetics in USA 2.2. INSULIN RESISTANCE 3.3. Problem with receptors,4.4. Chronic complications:^ Diabetes Mellitus:Diabetes Mellitus: Type II Over 15 million diabetics in USA- INSULIN RESISTANCE Problem with receptors, glucagonChronic complications:a)a) 10% type I a)a)b)b) 90% type II a)a) atherosclerosis b)b) renal c)c) Blindness 10% type I10%10% type I,90% type II atherosclerosisrenal failureBlindness neural capillaries; reasons unclearneural capillaries; reasons unclear type I, Group of DiseasesGroup of Diseasesfailure (diabetic retinopathy)(diabetic retinopathy) – (osmotic glucose,(osmotic glucose, ((↑↑ fatfat metab’mmetab’m/release) (^) glucagon levelsggkeeps blood glucose too highkeeps blood glucose too high gg /release),↓↓ Type II is a (^) – pericytesreabs’nreabs’n), &-pericytes lost aroundlevels,), &lost around is a
Figure 22Figure 22--19: Heat balance19: Heat balance
Homeostatic Balancing of BodyHomeostatic Balancing of Body 1.1. 2.2. 3.3. 1. Thermoregulatory Reflexes1. Thermoregulatory Reflexes (^) (^) Peripheral and body core receptorsPeripheral and body core receptors –senses changesenses change Hypothalamic thermoregulatory centerHypothalamic thermoregulatory center integrates & initiates:integrates & initiates:Shivering, nonShivering, non-(brown fat), vasoconstriction(brown fat), vasoconstrictiongg^ B. Thermoregulation:B. Thermoregulation:TemperatureTemperature -shivering thermogenesisshivering thermogenesis– – – NicotinicNicotinic AlphaAlpha • • brown fatbrown fat Figure 22Figure 22-Thermoregulatory reflexesThermoregulatory reflexes-20:20:
1.1. Eating2.2. Reversible reactions allow3.3. Energy is used for4.4. Metabolic rate changes with5.5. Insulin6.6. Glucagon6.6. Glucagon 7.7. Diabetes 8.8. Maintaining9.9. HypothalamicEating provides carbohydrates, proteins, & fats for metabolismReversible reactions allow interconversionEnergy is used for body heatstorage.storage.Metabolic rate changes with age, sex, lean musc, activity & diet.Insulin regulatesGlucagon regulatesGlucagon regulates Diabetes tolerance.tolerance.Maintaining homeothermy takesHypothalamic thermoregulatory center controls heat homeostasis. Endocrine Control^ Ch. 22: SummaryCh. 22: Summary provides carbohydrates, proteins, & fats for metabolismregulates anabolic is a major disease associated with insulinis a major disease associated with insulin - regulates catabolicregulates catabolichttp://www.sciencehttp://www.science-homeothermy takesthermoregulatory center controls heat homeostasis. Chapter 23 anabolic cell activities & glucose uptake in cells.body heat andcatabolic reactions & prevents hypoglycemia.catabolic reactions & prevents hypoglycemia.cell activities & glucose uptake in cells.interconversion of nutrients.age, sex, lean musc, activity & diet.and work: transport, synthesis,reactions & prevents hypoglycemia.reactions & prevents hypoglycemia.-groove.org/Now/Glucose.html groove.org/Now/Glucose.html≈≈work: transport, synthesis,50% of our energy.50% of our energy.of nutrients.- lack orlack or & of Growthof GrowthMetabolism