Fatty acids are broken down in the mitochondria to produce acetyl-CoA. The process is called beta-oxidation. Acetyl-CoA is then used to produce energy via the citric acid cycle pathway. Fatty acids cannot cross the mitochondrial membrane directly without the use of the carnitine shuttle.The process described in the question represents the carnitine shuttle pathway, which allows activated fatty acids (fatty acids with CoA attached) to cross the mitochondrial membrane so they can be broken down by beta-oxidation. Fatty acid synthetase activates the fatty acid on the outer mitochondrial membrane by attaching a CoA group. Carnitine acyltransferase 1 exchanges the CoA with carnitine forming fatty acyl carnitine. Fatty acyl carnitine is shuttled across the membrane through the carnitine transporter. On the inner side of the membrane, carnitine acyltransferase 2 removes carnitine and forms fatty acid-CoA which can then be processed by beta-oxidation.

Thiolase is an enzyme that performs a reaction forming acetoacetyl-CoA from two molecules of acetyl-CoA. This reaction is the first step in the process of converting acetyl-CoA molecules to ketone bodies.

Acetyl-CoA carboxylase catalyzes the committed step in fatty acid degradation - the step that forms malonyl-CoA. And so, in order to regulate fatty acid metabolism this is the enzyme that is most often controlled. Phosphorylating acetyl-CoA carboxylase inactivates it when it no longer needs to be functioning.

Phosphatidate is an intermediate in the synthesis of triacylglycerols and glycerophospholipids. This is simply because phosphatidate is the primary intermediate in lipid metabolism (which occurs in the synthesis of triacylglycerols and glycerophospholipids). More specifically, this intermediate is acylated to triacylglycerol through a fatty acid chain, and results in a glycerophospholipid product.

The correct answer is "Acetyl-CoA." The oxidation of fatty acids is activated by attachment to Coenzyme A to form fatty acyl-CoA, and the oxidation results in a shorter fatty acyl-CoA and acetyl-CoA. The acyl-CoA is oxidized in the citric acid cycle, where it is an important intermediate. Succinyl-CoA is also an intermediate in the citric acid cycle but is not a direct product of fatty acid oxidation. The shorter fatty acyl-CoA is oxidized further into FADH₂, but not as part of the citric acid cycle.

To answer this question, we'll need to keep in mind some of the highlights of beta oxidation. When a fatty acid is broken down by this method, the hydrocarbon chain is broken down two carbons at a time through a series of repeating reactions. These two carbons come off in the form of acetyl-CoA, with an additional generation of one molecule each of NADH and . Since we know the original chain we're starting with contains twelve carbons, we know that there will be six molecules of acetyl-CoA produced. Furthermore, in order to generate these six molecules, beta-oxidation must proceed five times. Thus, we are going to have five molecules of NADH and five molecules of . The acetyl-CoA generated from beta oxidation is able to enter the citric acid cycle. For each molecule of acetyl-CoA that goes through the cycle, 1 molecule of ATP, 1 molecule of , and 3 molecules of NADH are generated. Therefore, since six molecules will be sent into the citric acid cycle, there will be a total generation of six molecules of ATP, six molecules of , and eighteen molecules of NADH. Now, we need to add everything up. So far, we have six molecules of ATP. We also have five molecules of NADH from beta-oxidation, and eighteen from the citric acid cycle, for a total of twenty-three. We've also obtained five molecules of  from beta-oxidation, and another six from the citric acid cycle for a total of eleven. All of the NADH and  that was generated from these reactions can donate their electrons into the electron transport chain to generate ATP. The rule of thumb is that for every NADH,  molecules of ATP are produced. And for every molecules of ,  molecules of ATP is made. So, we have:

And if we add to this the six ATP that was generated directly by substrate-level phosphorylation in the citric acid cycle, that gives us a total of:

Palmitate is a sixteen-carbon chain and its beta-oxidation will produce 8 acetyl-CoA molecules, since each acetyl-CoA is two-carbons long. Glucose, on the other hand, will be broken down to form 2 acetyl-CoA molecules. Therefore, palmitate forms 4 times as many acetyl-CoA molecules. 

The oxidation of ethanol to acetaldehyde in the liver produces , leading to an elevated  ratio. Multiple enzymes responsible for fatty acid oxidation are under control of this ratio; they are active when there is more  an inactive when there is more . Thus, they become inactivated, and fatty acids are stored in the liver as triglycerides - this is why alcoholism leads to fatty liver disease. Free radicals can damage the liver and other tissues but do not directly inhibit these enzymes; neither does the ethanol molecule itself nor acetaldehyde

For this question, we're going to need to know a few things right off the bat.

First, it's important to know what the general "mission" of insulin is. Generally speaking, insulin is a hormone that helps the body out when there is ample energy available. For example, right after eating a meal, blood sugar levels are going to be fairly high. Thus, the body is in a state where it doesn't want to be breaking things down to provide energy. Rather, it wants to store the energy that it has just been given. This storage generally comes in the form of glycogen and fat.

Next, it's important to understand what acetyl-CoA carboxylase (ACC) does. As its name would suggest, it adds a carboxyl group onto acetyl-CoA. By doing so, it generates malonyl-CoA. This is a very important molecule that is used in the synthesis of fatty acids. Thus, when there is a lot of malonyl-CoA in the cell, it's likely that the cell wants to use it up to create fatty acids. Furthermore, in order to ensure that fatty acids aren't being broken down at the same time (which would be wasteful), malonyl-CoA also blocks the breakdown of fatty acids.

Equipped with this information, we can go ahead and piece together the facts as though it were a story. Insulin wants the body to store energy. It activates cellular receptors, which causes a downstream signaling event. Ultimately, this results in the activation of the enzyme ACC. This, in turn, generates a high amount of malonyl-CoA. The presence of high amounts of malonyl-CoA inside the cell gives the signal to make fatty acids and to also block their breakdown. So, all in all, acetyl-CoA becomes activated and the breakdown of fatty acids is inhibited.

Each round of beta oxidation yields one molecule of acetyl-CoA (along with one molecule of FADH₂ and one molecule of NADH). Both electron carriers feed into the electron transport chain, ultimately yielding ATP via chemiosmosis. Since the organic product of beta oxidation (acetyl-CoA) contains two carbons, nine rounds of beta oxidation are required to fully oxidize a fatty acid with a 20-carbon hydrocarbon tail. Recognize that it is NOT 10 rounds because the last round (9th) will cut the now 4-carbon hydrocarbon tail, yielding two acetyl-CoA molecules. As a rule, a fatty acid with a hydrocarbon tail of  of carbons undergoes  rounds of beta oxidation to be full oxidized.

Overall, for a fatty acid with 20 carbons in its hydrocarbon chain, 9 rounds of beta oxidation yielding 10 molecules of acetyl-CoA constitutes complete oxidation.