-oxidation of fatty acids yields large quantities of acetyl-CoA, all of which enters the citric acid cycle. The only intermediate in the citric acid cycle that can form back into glucose is oxaloacetate. It can be turned into phosphoenolpyruvate via phosphoenolpyruvate carboxykinase. 

In the first step of beta oxidation the enzyme acyl-CoA dehydrogenase forms a trans-double bond between the two carbons at the site that will eventually be cleaved.

First, one must know what the products of one cycle of the beta oxidation pathway are. Each cycle yields , _, 1 acetyl-CoA, and a fatty acyl-CoA molecule 2 carbons shorter than the original.

Therefore, an eighteen-carbon fatty acyl-CoA input can go through the beta oxidation cycle 8 times (the last round only a 2 carbon acetyl CoA remains, which cannot enter the beta oxidation pathway again). That means there are  molecules, 9 acetyl-CoA molecules, and  molecules that can be generated from an eighteen-carbon fatty acyl-CoA. 

It may be confusing to understand why there are only  and  molecules and 9 acetyl-CoA, but if one is solving a problem such as this for the first time, go through and draw out the products following each round of the beta oxidation cycle.

2.5 ATP on average can be formed from each  molecule, and 1.5 ATP from each   molecule through the electron transport chain. 10 ATP can be formed in total from one acetyl-CoA entering into the Krebs cycle (by the products of  and  ), along with one GTP molecule.

Therefore:

If taken into consideration, 2 ATP are needed to activate a fatty acid and allow it to enter into the mitochondria via the enzyme acyl-CoA synthetase.

Therefore, the toTal net yield is

For a quick reference, the following equations can be used:

Where  is number of carbons of an even numbered fatty acid chain.

For each round of beta-oxidation, two carbon atoms are removed from the fatty acid chain. These two carbon atoms come off of the chain in the form of acetyl-CoA. Additionally, high energy electron carriers in the form of NADH and  are also produced, thus making beta-oxidation a process that liberates a great deal of energy.

Since the fatty acid that we're starting with has a total of  carbon atoms, we can expect there to be a total of  acetyl-CoA molecules produced, since each of these contains two carbons from the fatty acid.

During beta oxidation of fatty acids, carbons are removed from the fatty acid chain two at a time. So when a fatty acid is composed of an even number of carbons (as most are) 4 carbons will be left at the end. This will be cleaved into two separate 2 carbon molecules - two acetyl-CoA molecules.

During beta-oxidation of fatty acids, carbons are removed from the fatty acid chain two at a time. So when a fatty acid is composed of an odd number of carbons, 5 carbons will be left at the end. This will be cleaved into two separate molecules - one with 3 carbons and one with 2 carbons. This is one acetyl-CoA molecule (2 carbons) and one propionyl-CoA molecule (3 carbons).

Fatty acids with an odd number of carbons are more common in plants and marine organisms than they are in mammals. When humans consume these organisms in their diets, they must metabolize them through beta oxidation. The end product of this reaction is propionyl-CoA rather than acetyl-CoA, which is formed during cleavage of two-carbon segments (fatty acids with an even number of carbons). Before entering the Krebs cycle, the propionyl-CoA must be transformed into succinyl-CoA.

Fatty acids are taken into the mitochondria to be broken down. This makes sense especially if you consider that the acetyl-CoA generated can be directly used in the citric acid cycle and oxidative phosphorylation immediately afterwards. Note that some beta-oxidation of fatty acids also occurs in the lysosome when the fatty acids chains are too long for the mitochondria. 

The basic pattern of saturated fatty acid catabolism is that the chain is broken down two carbons at a time by release of acetyl-CoA. So, the challenge for the cell is to turn a two-carbon alkyl group at the end of the chain into a thioester (remember, acetyl-CoA is . To do this, the cell first desaturates the chain (removes some hydrogens by oxidation) to form a double bond. Then, water is added across the double bond to form an alcohol. Thinking back to organic chemistry, remember we can oxidize an alcohol to get a carbonyl, which is exactly what the cell does. The result is a ketone which reacts with the thiol of CoA-SH to form the new thioester acetyl-CoA, which is removed from the chain in the process of its formation.

When plasma glucose is low (or when plasma glucose is inaccessible to cells as in diabetes) and glycogen stores have been depleted, the cells resort to oxidation of fatty acids for energy. Because the brain cannot utilize fat for energy, though, and because glucose is an important fuel source for other tissues as well, the liver begins to produce glucose from Krebs cycle intermediates like oxaloacetate. Once these begin to run low, Krebs cycle function slows, and acetyl-CoA from fatty acid oxidation builds up. The body's solution to this problem is to have the liver convert this excess acetyl-CoA into ketone bodies, which can be utilized by the brain and other tissues for energy.