1.  First, dihydrolipoate goes to the active site of dihydrolipoyl dehydrogenase, where it gets oxidized by FAD making it back into lipoate (making the FAD into FADH2). Then, the FADH2 is reoxidized into FAD by NAD+ (making it into NADH).

2. It is driven by the fact that each electron carrier has a higher standard reduction potential than the one it accepts the electron from driving it down all the way to oxygen, the one with the highest standard reduction potential.

3. ATP is generated by the proton pumping complexes, and NADH goes through complex one, which is a proton pump, while FADH2 does not get to go through it and instead goes through complex two, which is not a proton pump.

4.  ATP is used up to move pyruvate, phosphate, and ADP into the mitochondria for cellular respiration reducing the yield. Some of the protons could leak across the mitochondria's inner membrane reducing the yield. Some of the intermediates from glycolysis and the krebs cycle can be used for other pathways reducing the yield of ATP. For example, the Glucose 6-phosphate from glycolysis can be used in the pentose phosphate pathway if NADPH or 5 carbon sugars are needed more than ATP. For the Krebs cycle, its intermediates can be used to synthesize molecules such as amino acids and fatty acids instead of ATP.

5. Pyruvate dehydrogenase and citrate synthase are the enzymes that determine the rate of the citric acid cycle. Pyruvate dehydrogenase would be allosterically inhibited by ATP, acetyl CoA and NADH while it would be activated by NAD+ and CoA. Citrate synthase would be allosterically inhibited by succinyl CoA, NADH, and ATP.

6.First, citrate is transported by the tricarboxylate carrier to the cytosol in exchange for malate into the mitochondria. This however leaves the charges unbalanced as malate has a charge of 4c while citrate has a charge of 6c. Malate then has to be transported to the cytosol by a dicarboxylate carrier for inorganic phosphate into the mitochondria balancing the charge.

7.Citrate can be transported to the cytosol when NADH and ATP energy is readily available, so it will be okay if it is used for fatty acid synthesis.

8. Citrate inhibits phosphofructokinase, a key part of glycolysis, allosterically when it enters the cytosol (when ATP levels are high). This changes the binding from hyperbolic to an allosteric sigmoidal graph. However, when energy levels drop, AMP reverses the inhibition and citrate continues to be used by the TCA cycle to replenish the NADH and ATP and not inhibit PFK and glycolysis as a whole in the cytosol.

9. Seeds have energy stored in them as lipids, and when they start to germinate, the fatty acids are converted into carbohydrates where fatty acids are broken into acetate/acetyl CoA. The resulting acetyl-CoA is then used to make citrate, used in gluconeogenesis, and used in the glyoxylate cycle if no sunlight is present.

10. The glyoxylate cycle ends up making malate, oxaloacetate, and succinate as its end products. Both malate and oxaloacetate are used to make phosphoenolpyruvic acid which is the first substrate used in gluconeogenesis while succinate can be made into oxaloacetate via TCA cycle (which as stated above can make PEP).

11.First, the free fatty acids are converted into acetyl-CoA in the glyoxysome, which is going to be used in the glyoxylate cycle. As mentioned above, the cycle ends up producing the TCA intermediates succinate, malate, and oxaloacetate. Oxaloacetate is also transported out of the mitochondria as aspartate, which is then reconverted into oxaloacetate in the glyoxysome. This joins with the preexisting acetyl-CoA to make citrate. The cycle then completes itself with the malate being transported to the cytosol to be exposed to cytosolic malate dehydrogenase making it into oxaloacetate which is then subsequently used in gluconeogenesis. Succinate also is made by the cycle, and it is transported to the mitochondria where it enters the TCA cycle