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Chapter 27 (continued). Specific Catabolic Pathways:. Carbohydrate, Lipid & Protein Metabolism. 1. 2. 3. Fatty Acids and Energy. Fatty acids in triglycerides are the principal storage form of energy for most organisms.
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Chapter 27 (continued) Specific Catabolic Pathways: Carbohydrate, Lipid & Protein Metabolism
1. 2. 3.
Fatty Acids and Energy • Fatty acids in triglycerides are the principal storage form of energy for most organisms. • The energy yield per gram of fatty acid oxidized is greater than that per gram of carbohydrate oxidized.
b-Oxidation • five enzyme-catalyzed reactions • cleaves carbon atoms two at a time from the carboxyl end of a fatty acid.
b-Oxidation • Reaction 1: the fatty acid is activated by conversion to an acyl CoA; activation is equivalent to the hydrolysis of two high-energy phosphate anhydrides.
b-Oxidation • Reaction 2: oxidation of the , carbon-carbon single bond to a carbon-carbon double bond.
b-Oxidation • Reaction 3: hydration of the C=C double bond to give a 2° alcohol. • Reaction 4: oxidation of the 2°alcohol to a ketone.
b-Oxidation • Reaction 5: cleavage of the carbon chain by a molecule of CoA-SH.
b-Oxidation • This cycle of reactions is then repeated on the shortened fatty acyl chain and continues until the entire fatty acid chain is degraded to acetyl CoA. • b-Oxidation of unsaturated fatty acids proceeds in the same way, with an extra step that isomerizes the cis double bond to a trans double bond.
Energy Yield from b-Oxidation • Yield of ATP per mole of stearic acid (C18). Glycolysis TOTAL 36
Challenge Question • IF lauric acid (1) is metabolized through b-Oxidation, • what are the products of the reaction after 3 turns of the spiral? (1)
Confirming your knowledge • Which C-18 fatty acid yields the greater amount of Energy: • Saturated stearic acid? • Monounsaturated oleic acid?
Formation of Ketone bodies from lack of glucose • A little Glucose needed to fully run b-Oxidation β-Oxidation Formation of Ketone Bodies for Energy (Low glucose levels) headaches.. ?
Ketone Bodies, see p. 677-8 • e.g. acetone, B-hydroxybutyrate, and acetoacetate; • are formed principally in liver mitochondria. • can be used as a fuel in most tissues and organs. • occurs when acetyl CoA builds up • (due to limited glucose levels) • vs the amt. of oxaloacetate available • to react with it + take it into the • Citric Acid Cycle
Ketone Bodies are formed • for example when: • intake is high in lipids and low in carbohydrates. • diabetes is not suitably controlled. • Starvation occurs.
Challenge Question • What happens to the oxaloacetate produced from carboxylation of phosphoenolpyruvate? (i.e. where does it go and or where is it needed?) ?
Protein Catabolism Figure 27.7 Overview of Protein catabolism.
Nitrogen of Amino Acids • A. -NH2 groups move freely by Transamination • Amino acids transfer amino groups to a-ketoglutarate Glutamate . . .
Nitrogen of Amino Acids • B. Oxidative Deamination nitrogens to be excreted are collected in glutamate, which is oxidized to a-ketoglutarate and NH4+. • NH4+ then enters the urea cycle.
The Urea Cycle – Overview • a cyclic pathway that produces urea from CO2 and NH4+. For step details see p. 681-683
The Urea Cycle (cont.) (Urine)
Challenge Question • NH3 and NH4 are both H2O soluble and could easily be excreted in urine. • Why does the body convert them to Urea rather then excreting them directly?
Challenge Question 2 • What are the molecular sources of Nitrogen in Urea? Hint: see Urea Cycle Reactions Steps 1-2 and 3 p.681-682
Heme Catabolism • When red blood cells are destroyed: • globin is hydrolyzed to amino acids to be reused. • iron is preserved in ferritin, an iron-carrying protein, and reused. • heme is converted to bilirubin in spleen removed from blood (liver) • then transferred to gallbladder (stored in the bile) • finally excreted in the feces. • When balance upset [high bilirubin] in blood jaundice: (yellowing of face and eyes) • indicates Liver, spleen or gallbladder complications. . .
Final Challenge Question • Why is High bilirubin content in the blood an indication of liver disease?