CH 112 STUDY GUIDE: EXAM 3

For the third examination, you should be able to:

1. Draw the structures of pyruvate, lactate, acetic acid, acetyl group, acyl groups, acetyl CoA (abbreviating coenzyme A as CoASH).
2. Explain the overall functions of  pyruvate dehydrogenase, Kreb's cycle, and electron transport.
3. Show how glycerol obtained from triacylglycerol hydrolysis (fat mobilization) is a gluconeogenesis intermediate.
4. Explain possible methods of signal transduction utilized by cells.
5. Explain the effect of insulin/glucagon on triacylglyceride  metabolism.
6. Explain why acetyl CoA is not a gluconeogenic precursor.
7. Show the possible fates of the acetyl CoA and pyruvate  in metabolism
8. Explain the fate of NADH under anerobic and aerobic conditions.
9. Explain where the energy comes from in the Krebs cycle, and ox-phos. to drive the synthesis of ATP from ADP and Pi, which has a ΔG^o = + 7.5 kcal/mol
10. Explain a mechanism to uncouple oxidation and phosphorylation (ATP synthesis) in the mitochondria during aerobic metabolism.
11. Understand the "basics" of fatty acid oxidation and fatty acid synthesis
12. Understand the "basics" of ketogenesis and ketone utilization
13. Explain the role of CHO metabolism in triacylglyceride synthesis and mobilization.
14. Explain the link between CHO and triacyglyceride metabolism  in the liver ketogenesis
15. Explain the differences and metabolites of the liver, heart, muscle, and brain under various metabolic states.

Be able to give specific answers to the following questions:

1.  Fatty acid synthesis occurs in the cytoplasm and fatty acid oxidation occurs in the mitochondria.  But remember, the fatty acids for oxidation come from the blood and first must enter the cytoplasm before they are activated to acyl-CoA derivatives, and pass by way of the carnitine transport system, into the mitochondria.  How does a fatty acid in the cytoplasm know what to do?  Answer the following questions do find out.

1. Why does it make no biological sense for a freshly synthesized fatty acid in the cytoplasm to then enter the mitochondrial  matrix and get degraded?

2. To prevent this from happening, control mechanisms exist.  Explain why the following mechanisms of control of fatty acid oxidation and fatty acid synthesis make sense.
    

• the rate of fatty acid oxidation increases with increasing concentrations of fatty acids.

• the entry of fatty acyl-CoA molecules into the mitochondria through the carnitine transport system is inhibited by malonyl CoA.

• NADH inhibits the hydroxyacyl CoA dehydrogenase and Acetyl CoA inhibits the thiolase activity in the enzymes that degrade fatty acids in the mitochondria.

• citrate stimulates the acetyl CoA carboxylase enzyme of fatty acid synthesis.  (Note:  isocitrate dehydrogenase in the Krebs cycle is inhibited by high ATP.)

•  palmitoyl CoA inhibits acetyl CoA carboxylase.

• glucagon leads to the inhibition of acetyl CoA carboxylase.  (For this case, explain a mechanism!)

2.  Long term regulation of fatty acid synthesis also occurs.  This involves increasing the  synthesis of the enzymes involved in fatty acid synthesis within the cell (Acetyl coA carboxylase, fatty acid synthase complex.  The main site of fatty acid synthesis is the liver and adipose cell.  Explain if you agree with the following statements which refer to the liver: 

1. When an animal is fed high levels of glucose, the levels of these enzymes decrease. 

2. In an insulin-dependent diabetic animal, the production of these enzymes increases when the animal is given insulin.

3. During starvation, or diabetes associated with insulin deficiency, the levels of these enzymes decrease.