Transcript Slide 1

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; CO2
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 CO2 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 CO2, NADH, and other energy
compounds (ex. FADH2); final reaction produces oxaloacetate,
completing the cycle
– Two turns of the cycle per starting glucose molecule
• Oxidative Phosphorylation (the “payoff”)
– Oxidations of NADH and FADH2 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 H2O)
• 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 sugarcontaining 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