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Understanding Digestive Enzymes, Insulin, Glucagon, and Energy Use in Digestion - Prof. Na, Lab Reports of Physiology

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.

Typology: Lab Reports

Pre 2010

Uploaded on 08/18/2009

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4/28/2009
1
BIOL
BIOL
260260:
:
Human
Human
Physiolog
y
Physiolog
y
Spring Spring 2009 2009 WW, , Apr. 29, Apr. 29, 2009 2009
www.smccd.edu/accounts/sta
p
lesn/biol260www.smccd.edu/accounts/sta
p
lesn/biol260
pp
1.1. PrePre--Lab Lab WriteupsWriteups::Be sure to prepare Be sure to prepare beforebefore each each MondayMonday’s labs (for WHOLE week ’s labs (for WHOLE week
Mon. & Wed.!)!! Mon. & Wed.!)!! ------ (What? Why? How? are we doing in the lab?)(What? Why? How? are we doing in the lab?)
2.2. Monday Lab: Monday Lab: PhysioExPhysioEx 1717
3.3.
QUIZ #6 dueQUIZ #6 due
TONIGHT……!!!TONIGHT……!!!
3.3.
QUIZ
#6
due
QUIZ
#6
due
TONIGHT……!!!TONIGHT……!!!
4.4. Review sessions Review sessions TODAYTODAY, , 9:30am & 9:30am & 1:00pm 1:00pm – in Room 16in Room 16--204.204.
5.5. MT3MT3 Study guide Study guide is updated & posted!!! (is updated & posted!!! (ChsChs. 17, 18, 21, 22). 17, 18, 21, 22)
REVIEWREVIEW
1.1. **List and describe **List and describe digestive enzymesdigestive enzymes, , locationslocations in the GI tract, and each mechanism of in the GI tract, and each mechanism of
absorptionabsorption for for carbohydrates, fats and proteinscarbohydrates, fats and proteins during fed metabolism.during fed metabolism.
2.2. List and describe several List and describe several nervous and chemical signalsnervous and chemical signals that that regulate GIregulate GI function.function.
TODAY:TODAY: Students should be able to….Students should be able to….
1.1. Ch. 22:Ch. 22: Compare and contrast Compare and contrast fed and fasted statesfed and fasted states of metabolism in of metabolism in
regards to Carbohydrates, Fats, and Proteins.regards to Carbohydrates, Fats, and Proteins.
2.2. Outline the Outline the 4 possible fates (destinations) of lipids4 possible fates (destinations) of lipids in metabolism.in metabolism.
3.3. **Compare and contrast the activity of **Compare and contrast the activity of insulininsulin on different tissues during on different tissues during
(adipose skel m sc li er pancreas)(adipose skel m sc li er pancreas)
(adipose
,
skel m
u
sc
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li
v
er
,
pancreas)
.
(adipose
,
skel m
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sc
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li
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pancreas)
.
4.4. **Compare and contrast the activity of **Compare and contrast the activity of glucagonglucagon on different tissues during on different tissues during
fasting metabolismfasting metabolism (adipose, skel musc, pancreas, liver).(adipose, skel musc, pancreas, liver).
5.5. Compare and contrast the Compare and contrast the pathologies of Diabetes mellitus type 1 pathologies of Diabetes mellitus type 1 andand
type 2type 2. Describe causes, symptoms, and possible treatments.. Describe causes, symptoms, and possible treatments.
6.6. ** Compare and contrast the physiological (nervous, endocrine, vascular, ** Compare and contrast the physiological (nervous, endocrine, vascular,
metabolic) responses triggered by metabolic) responses triggered by hyperthermia & hypothermiahyperthermia & hypothermia..
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BIOLBIOL 260 1.1. 2.2. 3.3.3.3. 4.4.5.5. 1.1. www.smccd.edu/accounts/staplesn/biol260www.smccd.edu/accounts/staplesn/biol260 SpringSpring 2009List and describeList and describe absorptionabsorptionPrePre-–– Mon. & Wed.!)!! Monday Lab:Monday Lab: PhysioEx QUIZ #6 dueQUIZ #6 dueQUIZQUIZ #6 due TONIGHT……!!! Review sessionsReview sessions TODAYMT3MT3 Study guide Mon. & Wed.!)!! ----LabLab Writeups Study guide #6 dueWriteups: 260: forfor 2009 carbohydrates, fats and proteinscarbohydrates, fats and proteins : Be sure to preparedigestive enzymesdigestive enzymes REVIEWREVIEW---TONIGHT……!!!TONIGHT……!!!TONIGHT……!!!Be sure to prepare PhysioEx 17TODAY(What? Why? How? are we doing in the lab?)(What? Why? How? are we doing in the lab?) : Human is updated & posted!!! (is updated & posted!!! (Chs Human Physiology ,, 9:30am &9:30am & 1:00pm 17 ,, locationslocations beforebefore eacheach 1:00pm – WW,,during fed metabolism.during fed metabolism.in the GI tract, and each mechanism ofin the GI tract, and each mechanism ofPhysiology MondayMonday Chs. 17, 18, 21, 22) Apr. 29,Apr. 29, 2009 pp – in Room 16. 17, 18, 21, 22) ’s labs (for WHOLE week’s labs (for WHOLE week in Room 16- 2009 -204.204.

2.2. TODAY:TODAY: 1.1. Ch. 22: 2.2. Outline the3.3. **Compare and contrast the activity of4.4. Compare and contrast the activity of5.5. Compare and contrast the6.6. ** Compare and contrast the physiological (nervous, endocrine, vascular, List and describe severalList and describe several Ch. 22: regards to Carbohydrates, Fats, and Proteins.regards to Carbohydrates, Fats, and Proteins.Outline theCompare and contrast the activity of fed metabolismfed metabolismfed metabolismfed metabolism **Compare and contrast the activity of fasting metabolismfasting metabolism Compare and contrast the type 2type 2 ** Compare and contrast the physiological (nervous, endocrine, vascular,metabolic) responses triggered bymetabolic) responses triggered by. Describe causes, symptoms, and possible treatments.. Describe causes, symptoms, and possible treatments. Compare and contrastCompare and contrast 4 possible fates (destinations) of lipids4 possible fates (destinations) of lipids (adipose skel m sc li er pancreas)(adipose skel m sc li er pancreas)(adipose, skel musc, liver, pancreas).(adipose, skel musc, liver, pancreas). Students should be able to….Students should be able to….(adipose, skel musc, pancreas, liver).(adipose, skel musc, pancreas, liver). nervous and chemical signalsnervous and chemical signals pathologies of Diabetes mellitus type 1pathologies of Diabetes mellitus type 1 fed and fasted statesfed and fasted states hyperthermia & hypothermiahyperthermia & hypothermia insulininsulinglucagonglucagon on different tissues duringon different tissues during thatthat on different tissues duringon different tissues during regulate GIregulate GI in metabolism.in metabolism. of metabolism inof metabolism in function.function... andand

22.2) Changes in Metabolic Rate22.2) Changes in Metabolic Rate^ 1.1. Energy for temperature regulation^222 2. Energy for metabolic processes3.3. Energy use is measured by^. Energy for temperature regulation –Energy for metabolic processesEnergy for metabolic processesEnergy for metabolic processesEnergy use is measured by ConsumptionConsumptionConsumptionConsumption^ a)a) Transport^ b)b) Mechanical^ c)c) Chemical^ a)a) Calories in food (^ b)b) Respiratory Quotient Input = Output (+ storage)Input = Output (+ storage) 1.1. Basal metabolic rate (BMR) TransportMechanicalChemical Calories in food ( Respiratory Quotientconsumptionconsumption – –^ – – Basal metabolic rate (BMR)^ CalorimetryCalorimetry ( == V^ Body Energy:Body Energy: VCC/V/V^ OO workwork –workwork –^ ((1.0^ workwork – [#C per mol.[#C per mol. r 1.0 = pure CHO ( CalorieCalorie= pure CHO; 0.8 = – synthesis & storage– move molecules kilocaloriekilocalorie synthesis & storage– muscle contractionmove moleculesmuscle contraction rel’del’d / O ))^ = ratio of CO= ratio of CO / O ; 0.8 = prot^22^ ==^ OxygenOxygen cons’dcons’d]^ ↑↑1L H1L H^ prot; 0.7 = fat) ] – –^ ÆÆ^^22 workworkworkwork^ –^ prod’nprod’n to O I.D.I.D. catabolites^22 ; 0.7 = fat)^ O 1O 1 heatheat catabolites. ˚˚C)C) to O^22.

2.2. Modifying factorsModifying factors^ a)a) Body heat releasedb)b) Ob)b) Oc)c) CO a)a) Age & genderb)b) Lean muscle massc)c) Physical activity leveld)d) Diete)e) HormonesBody heat releasedOOCOAge & genderLean muscle massPhysical activity levelDietHormones^22 consumptionconsumption^22 productionproductiontiti

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

1.1. 222 2. Absorptive MetabolismAbsorptive Metabolism.^ C.C. Pathways shift to maintain energy for metabolismPathways shift to maintain energy for metabolismStorageStorageStorageStorage^ ““Fasted StateFasted State” →→→→ glucoseglucoseglucoseglucose in bloodin bloodin bloodin blood (mitochondria,(mitochondria,peroxisomesperoxisomes) ) →→→→ organs in needorgans in needorgans in needorgans in need^ ::”^ CatabolicCatabolic^ oror^ PostPost- Figure 22Figure 22-FastedFasted-metabolismmetabolism--statestate-7:7:

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

1.1.2.2. (not 3.3. Insulin release (rest & digest!!) 4.4. ↑↑(not active muscle Insulin release (rest & digest!!) ↑↑•••• a)a) Stimulated byb)b) Inhibited byb)b) Inhibited by a)a)b)b)c)c) glucose uptake in most cellsglucose uptake in most cells ANABOLISM:ANABOLISM: > 100 mg/> 100 mg/dL GLUT4GLUT4 Stimulated by parasympatheticInhibited by sympatheticInhibited by sympathetic ↑↑↑↑↑↑ active muscle)glucose use & storage (glycogenglucose use & storage (glycogen synthprotein synthesisprotein synthesisfat synthesisfat synthesis insertedinserted re:gg dL ( = 1 mg/ml) sympathetic/sympathetic/ ( = 1 mg/ml)(( parasympathetic on beta cells re:) ↑↑ggCa++ andCa++ and / catecholamines/ catecholamines )) catecholaminescatecholamines on beta cells ↓↓PiPisynth))

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:

  • Type 1:Type 1: Beta Cells destroyed – – (most commonly–– (most commonly INSULIN DEFICIENCYINSULIN DEFICIENCY GlucoseGlucose ( • • no insulin produced•• "melting flesh", ketosis, acidosis,•• no insulin produced"melting flesh", ketosis, acidosis, glucosureadiuresisdiuresis & coma “Honey“Honey- – – Bottom line: your cells are STARVING, though you are wellBottom line: your cells are STARVING, though you are well-tissue/tissue/biomolecule Beta Cells destroyed biomolecule breakdown -sweet siphoning/urinesweet siphoning/urine” & coma ( breakdown HyperglycemiaHyperglycemia autoimmuneautoimmune →→ ÆÆ chronic fasted state,chronic fasted state, osmotic effects worsen…………osmotic effects worsen………… !)!)glucosurea, - --fed!fed! )) ÆÆ lots oflots of,

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

A. Body Temperature Balance:A. Body Temperature Balance: 1.1. Metabolic heat production usually required2.2. Balance is very narrow range, usually Homeothermic Temp BalanceHomeothermic Temp Balance Metabolic heat production usually required to maintain balanceto maintain balanceBalance is very narrow range, usuallyhigher than environmenthigher than environment•• • ••• Usually need to balance heatUsually need to balance heatUsuallyUsually need to balance heat loss Thermoneutral zoneThermoneutral zone ““(no clothing)(no clothing) Thermoregulatory rangeThermoregulatory rangeHomeothermicHomeothermic need to balance heat : 82: 82--8686°”: 50”: 50- ° F losslossloss!! F-131131° !!!!!! ° FF

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