KIN 292 1st Edition Lecture 8 These are the notes from Professor Starnes lecture of Clinical Human Physiology These come from the slideshows provided by the professor and include extra notes and explanations Highlighted or bolded information are things that I believe to be information that is important to look over multiple times The notes in red are my personal additions and quotes of Professor Starnes from the class lecture Outline of Last Lecture I 3 3 Reaction Rates II 3 4 ATP The Medium of Energy Exchange continued from Friday III 3 5 Glucose Oxidation The Central Reaction of Energy Metabolism Outline of Current Lecture I 3 6 Stages of Glucose Oxidation Glycolysis finish last lecture the Krebs Cycle and Oxidative Phosphorylation II 3 7 Energy Storage and Use Metabolism of Carbohydrates Fats and Proteins Current Lecture These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute NADH enters an electron transport chain at the beginning FADH2 enters lower on the chain Mitochondria Krebs cycle where NADH is made citric acid cycle Outer membrane permeable Inner mitochondrial membrane metabolism Chemical to mechanical NADH enters at top FAD enters further down 3 sites on cytochromes to kick on protons For each set of protons kicked out will produce ATP Energy from NADH FADH2 transferred to electrochemical gradient which is then transferred to ATP when ATP Synthase is stimulated to open by elevated ADP concentration ATP synthase allows only H to ATP Synthase pass through just like mechanical box This is another example of the breakdown products of ATP stimulating its synthesis cytochrome oxidase last electron accepter end product will inhibit the movement of the cytochromes o2 isn t there means electron transport chain cannot happen regulator for ATP synthase 1 2 O2 required by both NADH and FADH2 but less ATP produced by FADH2 because of where it enters the chain Net reaction of electron transport NADH H 1 2 O2 NAD H2O energy FADH2 1 2 O2 FAD H2O energy ATP production per electron donor nadh makes 3 ATP fadh makes 2 atp this number is produced from the process in the last slide Overall reaction 10 NADH 10 H 2 FADH2 34 ADP 34 Pi 6 O2 10 NAD 2 FAD 12 H2O 34 ATP Overall reaction glucose 6 O2 38 ADP 38 Pi 6 CO2 6 H2O 38 ATP Fat Storage lipolysis and route to mitochondria Can you see why the rate of ATP production is slower than glucose oxidation We store about 2 000 kcal of glycogen in our body but the quantity of fat storage is unlimited If you consume more carbohydrate than you can metabolize or store almost all of the excess will be converted to fat Note central location of acetyl CoA all of the nutrients can produce it and it can be used to make all of the nutrients Similar story for proteins If you consume more protein than needed for protein synthesis the excess will be converted to fat or glycogen Note central location of acetyl CoA all of the nutrients can produce it and it can be used to make all of the nutrients ATP per molecule of glucose vs palmitate a 16 C fat C6H12O6 6O2 6CO2 38 ATP C16H32O2 23O2 16CO2 130 ATP Lots of ATP from fat but all of it comes from aerobic pathways inside mitochondria Cannot synthesize ATP in cytosol Why is ATP production so high in fats ATP per molecule of glucose vs palmitate a 16 C fat C6H12O6 6O2 6CO2 38 ATP C16H32O2 23O2 16CO2 130 ATP Lots of ATP from fat but all of it comes from aerobic pathways inside mitochondria Cannot synthesize ATP in cytosol Why is ATP production so high in fats Because they form many acetylCoA molecules Lots of AcetylCoA also means lots of citrate Krebs cycle which can signal glycolysis to slow down PFK inhibition because it is not needed as much Saves those precious carbohydrates when fat is able to provide more of the energy How do they make so many acetyl CoA s oxidation A 5 enzyme pathway located in the mitochon dria matrix Clips off 2 C s at a time Makes NADH FADH2 too