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NUTR 4550 Exam 2 Study Guide

by: Victoria Hills

NUTR 4550 Exam 2 Study Guide NUTR 4550

Victoria Hills
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This study guide contains all the notes on the 6 powerpoints from this unit.
Nutrition and Metabolism
Dr. Elliot Jesch
Study Guide
nutrition, metabolism, Jesch, unit, 2, two, study, guide, energetics, AMPK, food, regulation, exercise
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This 24 page Study Guide was uploaded by Victoria Hills on Sunday February 21, 2016. The Study Guide belongs to NUTR 4550 at Clemson University taught by Dr. Elliot Jesch in Spring 2016. Since its upload, it has received 158 views. For similar materials see Nutrition and Metabolism in Nutrition and Food Sciences at Clemson University.


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Date Created: 02/21/16
NUTR 4550 Exam 2 Study Guide Food Regulation Slide 2: Tissue-Fuels Used-Fuels Released Table ** Lactate released = Means incomplete oxidation of glucose (Pyruvate à lactate instead of pyruvate à acetyl CoA) • Brain: -­‐ Fuels Used: o Glucose: Main source of fuel o Ketone bodies o Lactate (When the plasma concentration is elevated) -­‐ Fuels Released: o Lactate -­‐ Brain uses about 120 g of glucose per day -­‐ Blood brain barrier does not allow most FA to be transported across so that’s why it will use ketone bodies instead (Glucose is #1 preference) -­‐ Ketone bodies review: Not very high in concentration in a normal state unless an individual is following a ketogenic diet (High fat, low carbohydrates) + under starvation states (When food isn’t eaten for about a week or longer the glucose levels decrease à Depleted hepatic and muscle glycogen so there is a switching of fuels to ketone bodies) • Skeletal muscle: -­‐ Fuels Used: o Glucose: Main source of fuel o Free FA o TAG o Branched-chain AA: Able to skip the liver when consumed and go straight to skeletal muscle o Lactate -­‐ Fuels Released: o Lactate o Alanine o Glutamine -­‐ Use of fuels depends on exercise: o High intensity at max: Glucose preference for energy and NOT fat -­‐ Cori Cycle: o Ex: Sprinting (High intensity) à Produce lactate that goes back to the liver to produce glucose à Back out to cells for energy -­‐ Glucose-Alanine cycle • Heart: -­‐ Fuels Used: o Free FA o TAG o Ketone bodies o Glucose o Lactate -­‐ Fuels Released: None o Holds onto fuels to be more efficient -­‐ Cardiac muscle is constantly beating (~70 bpm) so there needs to be a constant fuel supply—Why FA or TAG is preferred -­‐ Because the heart prefers FA, there is going to be a lot of mitochondria present in cardiac muscle • Liver: -­‐ Fuels Used: o AA (Partial oxidation) o Free FA o Lactate o Glycerol o Glucose o Alcohol -­‐ Fuels Released: o Glucose o Ketone bodies o Lactate (During absorptive phase) o TAG -­‐ AA is the liver’s primary fuel source • Intestines: (Enterocyte) -­‐ Fuels Used: o Glucose o Glutamine -­‐ Fuels released: o Lactate o Alanine • Red Blood Cells: -­‐ Fuels Used: o Glucose -­‐ Fuels Released: o Lactate -­‐ Do not contain mitochondria so there can’t be FA oxidation (Purely anaerobic respiration) • Kidney: -­‐ Fuels Used: o Glucose o Free FA o Ketone bodies o Lactate o Glutamine -­‐ Fuels Released: o Glucose (Renal gluconeogenesis important in prolonged starvation) • Adipose Tissue: -­‐ Fuels Used: o Glucose o TAG -­‐ Fuels Released: o Glycerol o Free FA o Lactate • Retina: Do not contain mitochondria so glucose is its main fuel source à Why see diabetics go blind when retina cells can’t take up glucose for energy Slide 3: AMP-activated protein kinase (AMPK) • AMPK is an intracellular regulator of fuel (Seen in most cells) • Low levels of fuel activate AMPK • Active AMPK = Phosphorylated • Inactive AMPK = De-phosphorylated • AMPKKs (Includes LKB, CaMKK, others) à Kinase protein that phosphorylates AMPK to make it active -­‐ Calmodulin dependent kinase: Has the phosphorylation function and is regulated by allosteric regulators: ghrelin, IL-6, calcium, AMP, ATP, P- creatine (Phosphocreatine) • Allosteric regulators of AMPKKs that ultimately affect the activation or inhibition of AMPK: a) AMP: -­‐ Increased AMP in the cell allosterically regulates AMPKK to phosphorylate AMPK (Active version) b) Ghrelin: -­‐ Increased ghrelin allosterically regulates AMPKK to phosphorylate AMPK -­‐ Hormone produced in the fundus of the stomach -­‐ Stimulates food intake -­‐ Some can be found in pancreas -­‐ Acts on the hypothalamus and affects NPY and AgRP c) Calcium: Increased levels stimulate AMPKK à phosphorylate AMPK d) IL-6: Increased levels stimulate AMPKK à phosphorylate AMPK e) ATP and P-Creatine: Low levels stimulate AMPKK à phosphorylate AMPK • Active (Phosphorylated) AMPK regulates other processes in the body: a) ACC (Acetyl CoA Carboxylase) – Isoforms ACC1 and ACC2 -­‐ Enzyme that initiates FAS by catalyzing acetyl CoA à Malonyl CoA -­‐ AMPK inhibits ACC -­‐ Energy is needed in the cell so acetyl CoA isn’t being used to make FA at this point -­‐ Inhibition of ACC à decrease in malonyl CoA levels (FAS precursor) -­‐ CPT1: o Carinitine transport protein (A transferase) located in the mitochondria that transports FA into the mitochondria from the cytoplasm for beta oxidation o Increased malonyl CoA levels inhibits CPT1 since malonyl CoA is a precursor for FAS à Don’t want to make and break down FA at the same time -­‐ Overall: Low energy levels (High AMP) activates AMPK à Inhibits ACC à Decreases malonyl CoA levels à CPT1 inhibition goes away à FA transported into the mitochondria for beta oxidation b) NPY and AgRP -­‐ Ghrelin allosterically regulates AMPKK to phosphorylate AMPK à Stimulates hypothalamic neurons à Stimulate NPY and AgRP to increase food intake and down regulate energy expenditure c) Rab-GAPs: Catabolic pathway -­‐ Active AMPK inhibits rab-GAPs -­‐ Rab-GAPs inhibit GLUT 4 translocation -­‐ Inhibition of rab-GAPs allows the translocation of GLUT 4 to come to the plasma membrane and take up glucose d) 6PFK2: Catabolic pathway -­‐ Active AMPK increases 6PFK2 in the heart -­‐ Leads to increase in glycolysis e) Muscle LPL/CD36 translocation: Catabolic pathway -­‐ Active AMPK stimulates LPL so that TAG à glycerol and FA in the muscle -­‐ CD36: Transport protein that brings FA through the plasma membrane for they hydrolysis of FA in the cell -­‐ Overall: Active AMPK up regulates LPL and CD36 to transport FA into the cell for break down to produce energy f) SREBP: Anabolic pathway -­‐ Sterol responsive element binding protein -­‐ 2 isoforms involved in lipid metabolism -­‐ Signaling synthesis of cholesterol or FA -­‐ Produced in the cytoplasm and goes to the nucleus where it functions in binding and expressing certain regions of DNA that produces mRNA and protein nuclear transcription factor g) HMG-CoA Reductase: Anabolic pathway -­‐ Enzyme in cholesterol synthesis -­‐ Active AMPK inhibits HMG-CoA reductase which down regulates sterol/isoprenoid synthesis (Want to make energy not build things) h) Glycogen synthase (GS): Anabolic pathway -­‐ Active AMPK inhibits glycogen synthase i) mTOR: Anabolic pathway -­‐ Protein involved with protein synthesis -­‐ Active AMPK inhibits mTOR -­‐ Branched chain AA are stimulators of mTOR Slide 4: mTOR (Know general process) • mTOR protein is active when cell wants to synthesize especially protein • Insulin (Growth factor) • IGF1 (Growth factors): -­‐ GH binds to GH receptors on the liver to produce IGF1 -­‐ IGF1 increases at not or in response to exercise • Insulin and IGF1 bind to tyrosine kinase receptor à Intracellular processes to activate mTOR • BCAA help regulate mTOR—Especially leucine that activates mTOR • Whey protein: Consume after workout -­‐ High in leucine -­‐ Stimulates mTOR to synthesize protein (Building muscle) • Low intercellular ATP and high AMP: -­‐ AMPK is active which causes mTOR to be down regulated -­‐ Don’t want to up regulate protein synthesis with mTOR when the cell needs energy • Hypoxia: -­‐ Regulator of mTOR -­‐ Low concentrations of oxygen inhibit mTOR • When mTOR is activated due to the binding of insulin/IGF2 à Cascade of events + inhibition of autophagy -­‐ Autophagy is a process involved with cell housekeeping -­‐ Cell cleans up damage to organelles, fixes misfolded proteins, etc. -­‐ Active mTOR inhibits autophagy (Don’t want to degrade proteins) Slide 5: Pancreas • Endocrine portion: Secretes insulin and glucagon (Focus) • Exocrine: Secretes digestive enzymes à Duodenum • Absorption of nutrients from the small intestine à liver • Pancreas is located right by the liver to detect what was just consumed in order to release corresponding signals (Anatomy of the organs is very important) • When a mixed meal is consumed, glucose is taken up by the pancreas by GLUT 2 and is trapped by the cell via phosphorylation à glucose-6-phosphate via glucokinase = Initiation of pathway stimulates the release of insulin from the pancreas • Amylin: Released in conjunction with insulin à Job is to signal the brain to regulate nutrient levels Slide 6: Glucose Homeostasis • Normal fasting range for blood glucose levels: 70-100 mg/dL • Consumption of a mixed meal with carbohydrate: -­‐ Insulin levels increase -­‐ Glucagaon levels decrease -­‐ Insulin binds to receptors on the liver -­‐ Glucose uptake by liver -­‐ Synthesis of glycogen -­‐ Increase in FAS -­‐ Down regulate gluconeogenesis to keep blood glucose range 70-100 mg/dL • Skeletal muscle: Fed State -­‐ Store glucose as glycogen -­‐ Take up excess glucose and make FA in adipose tissue and when glycogen stores are filled • Low levels of glucose: Fasted state -­‐ Decrease insulin levels -­‐ Increase glucagon levels -­‐ Acts on muscle and liver to increase gluconeogenesis and glycogenolysis -­‐ Muscle: Decrease glucose uptake and likely using glucose from glycogen + FA + ketone bodies Slide 7 • X axis: Gives the time after a meal • Fed and post absorptive state: Refers to right after a meal is consumed—30 minutes – 3 hours then get into fasted state • When glucose levels decrease, insulin levels decrease à Due to the uptake of glucose by GLUT 4 in adipose tissue and muscle (Want to keep range around 70- 100 mg/dL) • When there are elevated levels of glucose and insulin, see a decrease in glucagon Slide 8 • Insulin binds to tyrosine kinase receptor à Intracellular signaling of a cascade of events in the phosphorylation of proteins • Binding of insulin: -­‐ Up regulation of GLUT 4 translocation to the plasma membrane -­‐ Excess glucose à FAS -­‐ Glucose à glycogen synthesis (Glycogen synthase up regulated) Slide 9 • 7 transmembrane G protein couple receptor: -­‐ Receptor that glucagon and epinephrine binds to -­‐ Transverses the plasma membrane 7 times -­‐ Uses GDP protein complex in the cascade of events • Alpha subunit of GDP activates adenylate cyclase (An integrated protein in the plasma membrane) that increases cAMP levels à Increases protein kinase A that affects different processes downstream • Protein kinase A effects: -­‐ Glycogenolysis increase via protein kinase A phosphorylating glycogen phosphorylase (Active form) o Release of glycogen from liver à Heaptic glycogen is able to leave the liver o Skeletal muscle glycogen cannot release glycogen but releases glucose -­‐ Stimulates gluconeogenesis o CREB mediated transcription factor: Transcribes certain sections of DNA that are specific to certain proteins o Glucagon upregulates CREB through protein kinase A o CREB increases levels of gluconeogenic enzymes (Pyruvate carboxylase, PEP carboxykinase, fructose-1,6-bisphosphatase, and glucose-6-phosphatase) -­‐ Stimulates lipolysis o Up regulation of HSL that increases the release of FA and glycerol from adipose tissue o FA go to the liver to be converted to ketone bodies in the starved state o FA can also be packed into VLDL and be secreted to go towards beta oxidation in cells for energy Slide 10: Summary Slide • Insulin à Increases mTOR, glycogen synthesis, protein synthesis, TAG storage, gene transcription of ACC to produce malonyl CoA, inhibition of autophagy • Low glucose levels: cAMP increases to turn on PKA + break down glycogen, increases gluconeogenesis, VLDL synthesis, and ketone synthesis Slide 11: Figure 19.9 • In the morning: When one eats breakfast, can see an increase in glucose, lactate, and ketone bodies • Lactate: Incomplete oxidation of glucose; Cells aren’t 100% efficient with converting glucose to pyruvate to acetyl CoA • Ketone bodies: Concentrations are relatively constant à Assume person is healthy and not on a ketogenic diet • Glycerol: Concentrations are relatively constant • Amino Acids: Concentrations increase a slightly because a mixed meal was consumed • TAG: Concentrations increase • Overall: The body is exceptional in regulating these various components à Most levels decrease by about 2-3 hours after consuming the meal = Why we eat in phases Slide 12: Figure 19.10 • Figure shows how 90 g of glucose is portioned between different tissues • 15-20 g of glucose will go towards the brain -­‐ The brain oxidizes 120 g of glucose per day • Liver takes up about 20 go of glucose for glycogen storage • The majority of glucose goes to skeletal muscle because it is a large tissue—Will receive 20-45 g -­‐ 20 g goes towards oxidation -­‐ 45 g goes towards glycogen • Small amount of 2 g of glucose goes to adipose tissue • Ex: On ketogenic diet for 8 weeks: -­‐ Low carbohydrate, high fat -­‐ Brain would use ketone bodies -­‐ Liver: Makes the ketone bodies and is likely depleted of all glycogen stores -­‐ Maybe using a little bit of glucose -­‐ If the diet includes a little protein, the dietary protein will be used for energy -­‐ Skeletal muscle is likely using proteins and fat as energy source Slide 13: Figure 19.11 • Figure shows changes in glucose, insulin, and glucagon over days of starvation • At 40 days of starvation: The blood glucose level will not change • Most glucose is produced through gluconeogenesis • Pyruvate precursors: Alanine + carbons à Used to make glucose Slide 14: Figure 19.12 • As an individual moves into 7, 14, 21 days of fasting, can see an increased concentration of acetoacetate and beta hydroxybutyruate (Ketone bodies) Regulation of Fuel Utilization in Response to Exercise Slide 4: Muscle Fiber Types • Type 1 Red Fibers Slow Oxidative Fatigue Resistant: -­‐ “Red” because of how the muscle fiber stains when looking at histology -­‐ Has high levels of myoglobin (Transports oxygen in muscle cells) -­‐ Oxidative: Has high concentration of mitochondria -­‐ Contract very slowly -­‐ Found in muscles that can be used for excessive periods of time -­‐ Fatigue resistant: Takes a long time for these muscles to fatigue because of the high oxidative capacity -­‐ When exercising and using weights, slow twitch fibers are going to be recruited first and then as one gets tired, fast twitch fibers are recruited -­‐ ATP generated through aerobic respiration: Glucose à pyruvate à acetyl CoA à TCA cycle à intermediates à ETC à oxygen (Final electron acceptor) -­‐ Capillary density is high -­‐ Low glycolytic capacity: Anaerobic glycolysis (Pyruvate à lactate) is found more so in fast twitch fibers but still want glycolysis around for the slow twitch fibers -­‐ Creatine phosphate -­‐ Glycogen intermediate low: Slow twitch fibers are more oxidative so mainly using FA as fuel source (High TAG content) à Glycogen content is going to much lower as a result -­‐ Not a lot of force is produced by these slow twitch fibers à As a result, a 1 repetition max will be completed where one works up to one rep at the heaviest case possible (Fast twitch fibers create a lot of force) -­‐ Activity use: Mainly aerobic à Running, cycling, long-distance activities, standing walking -­‐ Calf muscles • Type 2A Red Fibers Fast Oxidative Fatigue Resistant: -­‐ In between slow and fast twitch muscle fibers -­‐ Fast, oxidative, and fatigue-resistant -­‐ Recruitment order: Intermediate -­‐ Seen with exercises from long-distance running to sprinting -­‐ Intermediate mitochondrial density -­‐ Intermediate oxidative capacity -­‐ Have many glycolytic enzymes for oxidative phosphorylation and anaerobic glycolysis -­‐ Creatine and glycogen stores are high in these muscle fibers -­‐ Fast contraction velocity • Type 2X White Fast Glycolytic Fatigable: -­‐ Very fast contraction velocity à Respond quickly -­‐ Fatigue rapidly -­‐ Stain white because have low levels of myoglobin -­‐ Recruitment order: Late à As one gets tired, these muscles are recruited later -­‐ Used for sprinting and short-term exercises -­‐ Myoglobin content is low: Don’t have a lot of mitochondria so don’t need to be carrying as much oxygen to here -­‐ More anaerobic for ATP production: Anaerobic glycolysis—pyruvate à lactate -­‐ Low capillary density -­‐ High glycolytic capacity -­‐ High creatine content -­‐ High glycogen content -­‐ Won’t use a lot of FA for fuel -­‐ Quad muscles • Genetic factor plays a role in determining what type of muscle fiber you have • 99.9% of mitochondria is derived from the mother • Able to change some of the fiber types with exercise à HIIT and sprint training can increase the level of 2A intermediate twitch fibers so there is a blend of oxidative and fast twitch fibers Slide 5: Figure 20.3 • Looking at energy expenditure • At rest, the energy expenditure in a marathon is much lower than in a sprint • Whole body and skeletal energy expenditure is about the same à Can conclude that skeletal muscle accounts for a large percent of the energy expenditure during exercise • HIIT: Energy expenditure is increased during and after exercise • Lean muscle plays a huge factor on whole body energy expenditure • Resistance training recommended for those who wish to lose weight and increase lean muscle mass Slide 6: Figure 20.4 • Looking at the duration of exercise at 70% VO2max • 70% VO2max: Volume of oxygen that you can consume at maximal capacity -­‐ Usually written in mL/kg/min -­‐ Average for females: 30-40 -­‐ Average for males: 40-50 • Figure is for males that had their VO2max measured for a baseline and then they ran then took blood samples -­‐ Blood samples showed plasma fuel concentration (What fuels were being used during exercise) • 0-120 (X axis): -­‐ Fuel sources started to change -­‐ Glucose presence started to decrease (Because it’s likely that the glucose was being used for energy) -­‐ Lactate changes by increasing at the start of exercise (Anaerobic respiration at this point) but then levels off around 120 -­‐ FA presence increased (Occurs especially as get into longer exercise times) • FA change the most because as glucose levels go down and get more in a steady state, FA can then be used and are released into the bloodstream from adipose tissue so FA concentrations increase in the blood • Glycerol levels increase: Mirrors the hydrolysis of FA from TAG • Increase the intensity of exercise: Ex: 90% VO2max -­‐ Won’t be using slow oxidative muscle—The shorter, 2X fibers are mainly used (Can’t withstand fatigue like slow oxidative) -­‐ Likely using the higher force -­‐ More reliant on glucose for HIIT and FA use decreases -­‐ Glucose coming from glycogen stores -­‐ Lactate levels increase Slide 7: Figure 20.5 • Figure gives data based on healthy, young individuals • As insulin decreases, glucagon increases à Catabolic in stimulating the release of glucose from the liver from hepatic glycogen (Levels out once reach recovery state) • Exercise itself is catabolic • Cortisol: Does not change that much because this is a steady state form of exercise shown -­‐ When exercise as one’s max and taking part in resistance training/sprints à Likely that there is an increase in cortisol • Norepinephrine and epinephrine increase mirror glucagon -­‐ Mobilizing energy stores -­‐ Increasing glycolysis -­‐ Increase FA concentrations -­‐ Using glycogen and glucose • Olympic athlete: Can have from 70-80 VO2max (Higher than average individual) • Overall: As one is exercising, ATP levels decrease and AMP levels increase à An intercellular signal will act when there is AMP present to activate AMPK by phosphorylating it via AMPKKs à downstream effects to help the cell obtain energy Slide 8 • Higher intensity exercise relies more on muscle glycogen • Low intensity exercise (40-35% VO2max or less) uses mostly FA -­‐ White area under the curve = plasma free FA • Moderate intensity exercise (50-60% VO2max): See an increase in muscle glycogen • Max VO2max (80% +): Most fuel is coming from glycogen levels à anaerobic glycolysis • Liver: 80-100 g of glycogen stored • Muscle: 300-500 g of glycogen stored à Some people can store up to 900 g depending on how much they have • More fat can be stored than glycogen because water is stored with glycogen and this takes up a lot of space • Fat is smaller and doesn’t take up as much space • If able to store as much glycogen as fat, individuals would be 4x the size they are now Energetics PPT 1 (2/12/2016) Slide 1: Energetics • Creatine phosphate is used in skeletal muscle when undergoing high-intensity exercise • Creatine can be found in food and supplements • Creatine is the initial main supply of energy from creatine stores (Animal protein stores) à ~ 30 seconds • Creatine-P + ADP à ATP + Creatine • Then: ATP à ADP + Pi • Creatine allows one to work more in an anaerobic environment for a longer period of time • Use glycogen next, depending on the intensity of the exercise and then lastly stored fat (TAG) from skeletal muscle or adipose tissue • At the same time, lactate is being made (Glucose à pyruvate à lactate) • Lactate can go to the heart and liver • Liver: Lactate à Cori cycle à produce glucose à Used by skeletal muscle again • Lactate isn’t bad but is associated with lower exercise performance • Insulin binds to tyrosine receptor to have GLUT 4 take up glucose in skeletal muscle • While exercising, GLUT 4 is stimulated to go to the plasma membrane without the presence of insulin • Lower intensity exercises mainly use FA Slide 2: Figure 21.2 • Energetics: Energy expenditure • Energy: The capacity to do work; Our bodies have the capacity to turn food into energy • Energy is the substrate of work • 4 types of energy: Electrical, chemical, osmotic, and mechanical • If there is carbohydrate, lipids, and AA present, ATP is being created via substrate level phosphorylation (Glycolysis and TCA cycle) and oxidative phosphorylation (ETC) • Energy is measured in Joules, kcals, and watts • Calorimetry is used to measure kcals • Calorie: Energy required to raise 1 g of water 1 degree C • 1000 kcal = 1 calorie • When something is oxidize, carbon dioxide and water are always the by products • Oxidation of glucose: Glucose + 6 O à2 6 CO + 2 H O +2heat (3.8 kcal/g) • In the figure, the thicker the line, the more energy required for the corresponding process • Heat is always given off so not efficient • See uncoupling in infants à Infants have brown adipose tissue that generates heat since they don’t have the development to stay warm and generate their own heat • Membrane transports 20-30% ATP sodium potassium ATPase (A lot of energy we create goes just towards maintain the sodium-potassium pump) • T3 and T4 are regulators Slide 3: Figure 21.3 • Figure of a mitochondria with the macronutrients at the top (Protein, glucose, TAG) • ATP synthase is used to make ATP—Oxidative phosphorylation • During oxidative phosphorylation, carbond dioxide and O 3 • Beta oxidation: Palmitic acid + 23 O à 26 CO + 16 H2O + heat2(9.3 kcal/g) -­‐ Palmitic acid requires more oxygen than carbon dioxide so get more energy per gram • Direct measuring of calories measures the heat produced by an individual • Indirect measuring of calories measures how much carbon dioxide is produced and oxygen is consumed • REE (Resting Energy Expenditure): Amount of energy needed to maintain basic metabolic function—Measured in kcal/day • RQ (Respiratory Quotient): VCO /VO 2 2 -­‐ At a volume of 1, carbohydrates are mainly used at rest (6 CO / 6 O 2 1) 2 -­‐ Can tell which sources of fuel the body is using with RQ -­‐ Ratio of CO2 produced to O2 consumed while food is being metabolized: RQ = CO 2 eliminate2 consumed -­‐ RQ of palmitic acid: 0.7 -­‐ Oxidation of macronutrients: o Fats: Lower o Proteins: Middle o Carbohydrates: Higher Slide 4: Electron Transport Chain (Figure 21.4) • Production of ATP comes after the ETC with ATP synthase • ETC functions to move hydrogen ions from the matrix of the mitochondria to the inner membrane space + • Complex I: Pumps 4 H into the inner membrane space • Complex III: Pumps 2 H into the inner membrane space + • Complex IV: Pumps 4 H into the inner membrane space • Start with NADH that interacts with complex I so that the released electrons move down complexes I-IV à A total of 10 protons is moved from the matrix to the inner membrane • Start with FADH tha2 donates electrons at complex II and moves protons at complexes III and IV à A total of 6 protons is moved from the matrix to the inner membrane space • It is required for 4 protons to make 1 ATP (Through phosphorylation of ADP in ATP synthase) • NADH: Generates a theoretical maximum of 2.5 ATP • FADH : G2nerates a theoretical maximum of 1.5 ATP Slide 5: Figure 21.5 • Figure demonstrates how the body captures and uses energy • Total energy intake: -­‐ Comes from food that is being consumed and all the energy contained within that food (Combustible energy value of foodstuff) -­‐ AKA measure heat generated from the combustion of food if it was set on fire to determine the total energy of the food • Digestible energy intake: -­‐ What is absorbed from the GI tract -­‐ Arrow between total energy intake and digestible intake: Offshoot indicating that some of the total energy intake is lost as feces (5-10%) • Metabolizable energy: -­‐ What is available for use by cells of the body or caloric value of foods -­‐ Arrow between digestible energy and metabolizable energy: Offshoot indicating that some digestible or absorbed energy is lost in urine (2-3%) • Caloric values of food: -­‐ Carbohydrate: 4 kcal/g -­‐ Protein: 4 kcal/g -­‐ Lipids: 9 kcal/g -­‐ Alcohol: 7 kcal/g • Comparison of metabolizable energy to the combustible energy (total energy intake) of food: -­‐ The difference is off by a different percentage for each food -­‐ For carbohydrates and lipids: Metabolizable energy is close to the combustible energy (original total energy intake) -­‐ For protein: Metabolizable energy is off by about 25% compared to the combustible energy (original total energy intake) • Moving down the diagram: Metabolizable energy (100%) -­‐ Have heat loss when energy is being used due to biochemical inefficiency of converting energy into ATP -­‐ 60% of the metabolizable energy is lost as heat -­‐ This is not really considered a loss since the heat is necessary to maintain body temperature à Otherwise, enzymes would not function as well above or below 98.6 degrees F • Energy available to couple work (40%) -­‐ Energy converted to high-energy bonds of ATP -­‐ Have heat loss due to the biochemical inefficiency of coupling ATP to work -­‐ Where ATP is being utilized and the high energy phosphate bonds are being broken to perform work -­‐ 24% of the energy available to couple to work is lost as heat • Energy actually used to accomplish work (16%) -­‐ Includes mechanical work such as respiration and circulation, transport work, synthetic work, and muscle contraction -­‐ 12% of the energy actually used to accomplish work goes towards the dissipation of heat in the body as a consequence of internal work and muscle contraction to generate force for external work • External work done on the environment (2%) -­‐ Energy lost as heat (Ex: due to friction) or temporarily stored in the environment as non-heat energy as a consequence of external work -­‐ (Goes to 0%) • Overall, a relatively small amount of energy from food goes towards producing or using ATP • The inefficiencies and heat production are important • When the body starts to get too warm, it dissipates heat so that the body temperature doesn’t rise too high Slide 6: Electron Transport Chain, ATP Synthase, and UCP • In the electron transport chain, protons are moved from the matrix to the inner membrane space • ATP synthase makes ATP by shuttling protons back through the enzyme complex to produce energy for the phosphorylation of ADP à ATP • UCP: Uncoupling protein -­‐ Where in the mitochondrial membrane protons are leaking into the matrix of the mitochondria from the inner membrane space -­‐ Seen as an inefficiency but this is important in maintaining body temperature since there is some heat generation when the protons leak into the matrix -­‐ Especially important for babies: o Necessary to generate heat without movement – Uncoupling proteins allow babies to keep their proper body temperature since they aren’t able to maintain their own temperature yet o Evolutionary link: People that lived in cold climates long ago didn’t have the proper outwear à Uncoupling proteins were up regulated as a result to allow for more leakage of protons Energetics PPT 2 (2/15/2016) Slide 2: Figure 21.7 • Figure shows the generation of fat cells from adipocytes • On the right: There is a precursor for one white adipocyte and pre-adipocyte differentiation -­‐ After differentiation, the adipocyte is able to store fat and energy • On the left: There is a precursor for brown adipocyte and skeletal myocyte -­‐ Left arrow: Myogenic determination factors à Skeletal myocyte -­‐ Right arrow: Adipocyte determination factors à Brown adipocyte • White Adipocyte: -­‐ One large lipid droplet • Brown Adipocyte: -­‐ Contains more mitochondria -­‐ Smaller lipid droplets -­‐ Generate heat -­‐ Able to store lipid for energy but more so thought of as a heat generating cell -­‐ Mitochondria have the uncoupling proteins that allow the leakage of protons from the inner membrane space à Generation of some heat • Arrow from white to brown adipocyte-like cell: -­‐ White adipocyte can go through browning through some environmental cues (Ex: Cold weather) -­‐ Browning of fat tissue develops more smaller lipid droplets that generate more mitochondria -­‐ Contributes to helping maintain body temperature • Infants: -­‐ Contain more brown adipose tissue -­‐ As humans age and get bigger, we are able to more easily maintain body heat -­‐ Therefore, less energy needs to be put into maintaining body temperature • Other consequences of brown adipocytes or brown adipocyte-like cells: -­‐ Have uncoupled the transportation of protons from the matrix into the inner membrane space for ATP production -­‐ Now, protons are pumped into the mitochondria to make heat (Not getting anything out of it traditionally like ATP) -­‐ Related to a possible link to weight maintenance: Increase uncoupling proteins and therefore heat production à Use more energy as a result and not produce more ATP Slide 3: Figure 21.8—Alternative Process in Generating Heat for Body Temperature Maintenance • Fructose-6-phosphate à Fructose-1,6-bisphosphate via PFK -­‐ Reaction consumes 1 ATP to generate ADP • Fructose-1,6-bisphosphate à Fructose-6-phosphate via fructose bisphosphatase -­‐ Remove phosphate group and generate inorganic phosphate instead of going back to ATP -­‐ Consume water too • Bottom right: Net effect—ATP + H O à ADP + P + Heat 2 i -­‐ Alternative process that can generate some heat -­‐ Relates to maintain core body temperature Slide 4: Figure 21.9 • Figure shows the breakdown of how energy expenditure is distributed throughout the course of one day (BEE, TEF, and EEPA) • BEE (Basal Energy Expenditure): -­‐ Minimum amount of energy required to keep an individual alive- ~1,500 kcal/day -­‐ Nervous system, heart beating, transport systems, glycolysis, beta-oxidation, TCA cycle, etc. -­‐ Measure BEE in a sleeping state • REE (Resting Energy Expenditure): -­‐ When a person is generally awake but resting -­‐ Slightly higher than BEE • TEF (Thermic Effect of Food): -­‐ ~200 kcal/day -­‐ Digestion, absorption, mastication (Chewing with some muscular contraction), GI tract movement -­‐ Digestion: Includes production of enzymes and hormones that facilitate digestion, regulation, and metabolism -­‐ Absorption: Includes most nutrient transporters by sodium-potassium pumps that facilitate transport -­‐ Assimilation: Utilization of nutrients and cells by tissues o Ex: Lipids: Uptake into adipose tissue or muscle + stored as TAG o Ex: Glucose à glycogen -­‐ All nutrients contribute towards TEF, but the biggest contributor is protein -­‐ Protein TEF: o In terms of energy, protein = 4 kcal/g (This is the metabolizable energy) o Oxidizable energy = 5.4 kcal/g o Some energy is inherent to AA/proteins with the amine group o When harvesting energy from AA, protein, body can’t use the energy in the bond of the amine group o Breaking down AA à deamination so the amine group is lost as NH 3 o Therefore, AA metabolism isn’t as efficient as lipid and carbohydrate • EEPA (Energy Expenditure Physical Activity): -­‐ ~750 kcal/day comes from any form of physical activity (Walking, talking, etc.) -­‐ Most likely less than 750 kcal/day though -­‐ Moderate- highly active people will burn 750 kcal/day • GI Tract: Major fuel source is AA Slide 5: Figure T21.1 • Complete Oxidation of Food Component by Burning: -­‐ If the food is set on fire, able to measure the amount of energy gained from that nutrient -­‐ Carbohydrate: 4.1 kcal/g -­‐ Fat: 9.3 kcal/g -­‐ Protein 5.4 kcal/g • Complete Oxidation of Absorbed or Stored Fuel in Body: -­‐ Carbohydrate: 4.1 kcal/g -­‐ Fat: 9.3 kcal/g -­‐ Protein: 4.2 kcal/g à *Shows how there is some inefficiency with using protein as an energy source in comparison to carbohydrate and fat • Physiological Fuel Value of Consumed Foodstuff (Some energy is lost as heat, through feces, urine, etc. so this gives how much energy the body can actually use) -­‐ Carbohydrate: 4 kcal/g -­‐ Protein: 4 kcal/g -­‐ Fat: 9 kcal/g • RQ (VCO /VO ) of fat, protein, and carbohydrate: a) Fat: RQ of 0.71 2 b) Protein: RQ of 0.8 c) Carbohydrate: RQ of 1 *Think of these values generally as non-protein RQ à In most cases, protein isn’t being used as an energy source; Energy macronutrients are generally held to carbohydrate and lipids • When will see protein used as an energy source: -­‐ Prolonged starvation -­‐ Individual on a diet to lose weight -­‐ Individual on a specific diet that is low in carbohydrate • Can measure the nitrogen in urea to determine how much protein is catabolized à Assume no protein oxidation though most of the time Slide 6: Figure 21.11 • Figure demonstrates the breakdown of energy as one ages • Distribution of RMR (Resting metabolic rate) on the y-axis and age on the x-axis • Brain: Changes seen -­‐ RMR value decreases with age -­‐ Infants require a lot of energy use in the brain initially (Nervous development) • Muscle: Changes seen -­‐ RMR value decreases with age -­‐ Significant muscle growth occurs around puberty • Liver: Changes seen -­‐ RMR value increases with age -­‐ Increase due to detoxification à Toxins in the body start picking up especially around the age of 21 when drink more so energy needs to be devoted to detoxification -­‐ Also due to regulating the whole body energy status—Storing and using glycogen, synthesizing and breaking down FA, ketone body production -­‐ Efficiency with maintain body heat • Heart, kidney, and adipose tissue remain relatively constant -­‐ As long as the heart betas, the kidneys are always filtering blood (Function does not change) -­‐ Adipose tissue à Born with it, live with it, and die with it; Doesn’t require a lot of energy in storing fat • Everything else: Slightly decreases with age Slide 7: Figure 21.12- Whole Body RMR vs. Liver, Kidney, Brain, and Heart RMR across a life-span • Figure shows how RMR changes with time • As an infant, a lot of energy is expended per kg of body weight à Due to dissipating body heat especially • As one ages, the energy expended decreases per kg of body weight • Power of ¾: 3/4 -­‐ Across most mammals, you are able to take bodyweight to get an estimation of body expenditure -­‐ As the bodyweight value gets larger, a smaller number results for the RMR à AKA a small number to ¾ = more kcal/kg body weight vs. a large number to ¾ = less kcal/kg body weight -­‐ As our bodies get bigger with age, they get more efficient • Liver, kidney, brain, and heart: -­‐ All combined remain relatively constant across the life span -­‐ Liver RMR goes up -­‐ Brain RMR goes down -­‐ Heart goes up -­‐ Kidney stays about the same -­‐ Therefore, the sum of all of these = RMR remains about the same so the same amount of energy (~350 kcal/day) is used by the vital organs to function with age -­‐ Everything else drops off significantly Energetics PPT 3 (2/17/2016) Slide 2: Figure 22.1 • Energy balance: Energy in = energy out • Positive energy balance: Energy in > energy out à Increase in energy stores to maintain energy balance • Negative energy balance: Energy in < energy out à Decrease in energy stores to maintain energy balance Slide 3: Figure 22.1- Estimate of body stores • TAG: -­‐ Stored in adipose tissue -­‐ 140,000 kcal à kcal from this is regularly used for energy production • Protein: -­‐ Stored in muscle -­‐ 25,000 kcal is associated with muscle -­‐ Generally not used for energy production unless one is on a diet to lose wait or in the starvation state • Glycogen: -­‐ Stored in liver and muscle -­‐ 1,400 kcal is associated with this tissue -­‐ Used all the time especially in the liver to maintain blood glucose concentration • Glucose or lipid: -­‐ Stored in body fluids -­‐ Lipid in the blood is more dependent on excess carbohydrate and fat consumption Slide 4: Figure 22.2 • Figure shows fat stores on the bottom, protein stores in the middle, and carbohydrate stores on top • Energy in is on the left and energy out is on the right of the energy stores • 71% of daily oxidation comes from carbohydrate storage à Because carbohydrate is the preferred source of energy in the body • <1% of daily oxidation and nutrient balance comes from fat • Carbohydrate oxidation is for the brain or RBC especially, and lipid oxidation is for different pathways in generating ATP Slide 5: Figure 22.2 Slide 6: Figure 22.3- Basic Overview of Energy Balance • Left side: System energy balance • Right side: Controller of central nervous system • Figure shows what is going on to maintain body’s energy status and NOT what is regulating body weight/composition • Energy balance is to make sure that an individual has enough energy to carry them throughout the day • Energy balance means that all the inputs and outputs should come out equally • Various peptides, hormones, and vagal afferents work to control inputs to control changes of output in relation to changes in food intake and energy expenditure Slide 7: Figure 22.5 • Hormones and regulating peptides function to control energy status within the body • Consumed meal: -­‐ Glucose, AA, and FA nutrients come into the body and circulate -­‐ Sensing of these nutrients -­‐ Consuming a meal leads the brain to signal inhibition of anymore food intake (Slow down) -­‐ Overall: The GI tract and circulation of the nutrients in the blood signals the body to slow down consumption • Adipose: -­‐ Contains leptin hormone that signals inhibition of food intake -­‐ Leptin production is directly produced to the fat content in the body à The more fat, the more leptin produced to signal a reduction in food intake -­‐ Leptin is not dependent on the transport of FA or the storage of TAG -­‐ Long-term energy sensor -­‐ Obese Individuals: May have inborn error in leptin production or receptor, etc. • Pancreas: -­‐ Insulin, amylin, and PP (Peptide P) -­‐ Insulin focus à Glucose presence increases insulin production à downstream events with one being inhibition of food intake • GI Tract (Small Intestine): -­‐ CCK, PYY (Peptide YY), GLP-1, OXM -­‐ Hormones produced within the GI tract that signals the body to reduce food intake • Stomach: -­‐ Ghrelin -­‐ Produced in the fundus of the stomach -­‐ Only hormone that signals an increase in food intake • Emphasis is placed on inhibition of food intake rather than activation: -­‐ From an evolutionary standpoint, one is always going to want to eat -­‐ Too much of anything can be damaging to the body -­‐ Reason may not have even been discovered Slide 8: Figure 22.3 • Table describes hormones that have an effect on eating + where they are produced • Glucagon: Decreases with food consumption • Insulin: Signals decrease in food intake • CCK from the GI tract signal decrease in food intake • Ghrelin signals increase in food intake Slide 9: Figure 22.6 • Top Portion: Figure A—Orexigenic pathway -­‐ Orexigenic pathway: Stimulates food intake -­‐ Aanorexigenic pathway: Inhibition of food intake -­‐ More adipose tissue (Larger adipocytes shown in A than in B)à More stored energy à Increase in leptin production -­‐ Pancreas: o More adipose tissue à More food consumed à Insulin up regulated -­‐ NPY and AgRP proteins produced in neurons o Ultimately signal changes in appetite o Increased insulin and leptin down regulate NPY and AgRP o Less NPY à Less binding to orexigenic neurons o Because AgRP is not present as a result of inhibition by increased leptin and insulin, MSH is able to bind to the receptor to signal the anorexigenic pathway -­‐ Overall: Increased leptin/insulin à Inhibition of producing NPY and AgRP à Less signaling of the orexigenic pathway and signaling by MSH for the anorexegenic pathway to reduce food intake and increase energy expenditure • Bottom Portion: Figure B—Anorexigenic pathway -­‐ Less adipose tissue (Smaller adipocytes shown in B than in A) à Less stored energy à Decrease in leptin production -­‐ Decrease in insulin production from the pancreas -­‐ NPY and AgRP proteins o Increase in NPY à Binding of the receptor à Stimulate orexigenic neurons à Increased food intake and decrease energy expenditure o AgRP is present and blocks the receptor of the anorexigenic pathway so MSH cannot attach to it Energetic PPT 4 (2/19/2016) Slide 2: Figure 23.1- Functions of Adipose Tissue • Adipose tissue produces hormones like leptin that signals long-term energy status • Produces eicosanoids, complement factors, growth factors, cytokines, enzymes/proteins • Overall: Adipose tissue has other functions than just storing energy Slide 3: Figure 23.1- Weight Categories • Children: Based on percentiles -­‐ Problem because percentiles can change -­‐ Because children’s weights have been increasing à Percentiles have incthased -­‐ <5 percentile = Underweight -­‐ 5 -84 percentile = Healthy -­‐ 85 -94 percentile = Overweight th -­‐ >/= 95 percentile = Obese • Adults: Based on BMI -­‐ Absolute ranges -­‐ Not a good indicator of how healthy a person is because composition not taken into account -­‐ <18.5 kg/m = Underweight 2 -­‐ 18.5-24.9 kg/m = Healthy -­‐ 25-29.9 kg/m = Overweight -­‐ 30-34.9 kg/m = Obese class I 2 -­‐ 35-39.9 kg/m = Obese class II -­‐ >/= 40 kg/m = Obese class III


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