What are Glycolysis, Fermentation, and Aerobic Respiration? Glycolysis: breakdown of glucose (6C) into two moles of pyruvate (3C) –Occurs in the cytoplasm of all cells –Consists of 10 steps, each catalyzed by a different enzyme –Net gain of 2 ATPs (2.2% potential energy of glucose); nicotinamide adenine dinucleotide (NAD + ) required and NADH produced Fermentations (Anaerobic Conditions) –Lactate Fermentation: pyruvate from glycolysis reduced to lactate; occurs in muscles when starved of oxygen; bacteria produce lactate in yogurt and some cheeses –Alcohol Fermentation: pyruvate converted to ethanol via ethanal; CO 2 byproduct; used in production of wine –Oxidation of NADH to NAD + allows continued gylcolysis The Mitochondrion (Site of Aerobic Respiration in Eukaryotes) –Evolved from aerobic bacteria (have ATP synthase in membrane) –Aerobic Respiration: oxygen gas allows complete oxidation of glucose and production of 36 ATPs (~40% potential energy of glucose)

Figure 9.9a

Figure 9.9b

Figure 9.8

Figure 9.18

What are the Processes Involved in Aerobic Cellular Respiration? The Transition Reaction (pyruvate  acetyl CoA) –Acetyl Coenzyme-A: “central character” in metabolism (can be produced from carbohydrates, lipids, and certain amino acids) –Pyruvate converted to acetyl group (2C); loss of CO 2 molecule –Coenzyme-A (CoA): a large thiol derived from ATP and pantothenic acid (derived from thiamine and riboflavin); binds to acetyl group at the thiol group (-SH) of CoA; complex enters mitochondrion The Citric Acid Cycle (Krebs Cycle, TCA Cycle) –Acetyl group condensed with oxaloacetate (4C)  citrate (6C); series of oxidation reactions produce CO 2, NADH, and other energy compounds (ex. FADH 2 ); final reaction produces oxaloacetate, completing the cycle –Two turns of the cycle per starting glucose molecule Oxidative Phosphorylation (the “payoff”) –Oxidations of NADH and FADH 2 coupled to the production of ATP –Series of electron transport reactions produce ATP; final electron acceptor is molecular oxygen, which is used to produce water –Involves several enzymes, proteins in the mitochondrial inner membrane, H + pump, and H + reservoir between the membranes

Figure 9.10

Figures 9.11 and 9.12

Figure 9.16

Figures 9.14 and 9.15

Figure 9.17

How are Lipids Used as an Energy Source? Lipid Metabolism –Fats emulsified by bile in duodenum Bile: micelles consisting of bile salts, lecithin, cholesterol, proteins, and inorganic ions –Lipases from pancreas hydrolyze triglycerides to monoglycerides and fatty acids –If energy needed, fatty acids degraded to enter Krebs Cycle, if not, triglycerides re-formed and stored in adipocytes Fatty Acid Degradation –Fatty acids degraded to acetyl-CoA by β-oxidation Cycle (involves sequential loss of acetyl groups from carbon chain of fatty acid) –Energy yield depends on length of carbon chain (ex. 16C palmitic acid results in 129 ATPs, ~3.5x more than glucose) –Ketoacidosis: results if oxaloacetate in short supply; acetyl-CoA converted into ketones, which are weak acids; can occur due to starvation, low-carbohydrate diet, or by uncontrolled diabetes Fatty Acid Synthesis (via sequential additions of 2C groups) –Excess acetyl-CoA used to synthesize fatty acids, which are then stored as triglycerides

Figure 9.20

How are Proteins Used as an Energy Source? Digestion of Proteins –Proteins can supply energy, but not their primary function (most amino acids used for protein synthesis) –Body can burn muscle protein if starved Degradation of Amino Acids –Amino group transferred to a keto acid acceptor to form new amino acid (α-ketoglutarate  glutamate, which enters the Krebs Cycle) Aspartate from diet  oxaloacetate (needed in Krebs Cycle) Alanine from diet + α-ketoglutarate  pyruvate and glutamate –Amino acid carbon skeletons enter glycolysis or Krebs Cycle after oxidative deamination of amino group (requires NAD + and H 2 O) The Urea Cycle –Ammonium ions (toxic) result from oxidative deamination of amino acids  converted into urea, which is excreted in urine –Occurs in mitochondria and cytoplasm –Unusual amino acids produced as intermediates (ornithine, citrulline)

How are Glucose and Glycogen Synthesized? Gluconeogenesis (the synthesis of glucose) –Occurs during starvation to keep the brain and red blood cells supplied with glucose, and occurs following exercise (Cori Cycle: lactate converted to glucose, which is re-supplied to muscle tissue) –Occurs in the mammalian liver; other starting materials include glycerol, and most amino acids Glycogenolysis (the degradation of glycogen) –Glycogen stored in liver and muscles, but only liver-based glycogen used to supply blood (and brain) –Glycogen degraded to supply blood glucose in response to hypoglycemia (via glucagon levels) or threat (via epinephrine) Glycogenesis (the synthesis of glycogen) –Stimulated by hyperglycemia (via insulin levels) –Insulin acts as an inhibitor of glycogen phosphorylase, and stimulates glycogen synthase and glucokinase

Figure 45.12

What are the Effects of Insulin and Glucagon on Cellular Metabolism? Insulin –Produced by β-cells of the islets of Langerhans in the pancreas; secreted when blood glucose levels high (ex. after meals) –Increases cellular uptake of glucose from blood Target cells mainly liver, adipose, and muscle cells (with membrane receptors) –Activates biosynthesis and inhibits catabolism: stimulates glycogen synthesis, protein synthesis, and inhibits breakdown of glycogen, synthesis of glucose, and breakdown of triglycerides Glucagon: opposite effects of insulin –Produced by α-cells of the islets of Langerhans Diabetes mellitus (inadequate production of insulin) –Symptoms: odor of acetone on the breath; large amounts of sugar- containing urine; weakness, coma –Lipid metabolism increases since most glucose excreted in urine; shortage of oxaloacetate can lead to ketoacidosis –Treated by insulin injections, pancreas transplants, and more recently, with adult stem cells