First of all, there's a logical fallacy here - are you saying I said endocrinological problems are responsible for all cases of obesity?

Secondly, if you're making a claim like that, there are a lot of things you don't understand about the human metabolism (burning fat isn't as simple as boiling a kettle in terms of thermodynamics), so here's a crash course in case you aren't trolling.

The most important thing for your body, especially in fasting, is to produce glucose to supply the brain. When you start fasting, there are three stages that ensue.

First, you use the most readily available source of glucose you have - glycogen deposits in your liver. It's a simple matter of chopping the glycogen into the units it is composed of - molecules of glucose - and releasing them into the bloodstream (the mechanism is really fun and fascinating but I won't go into too much detail).

When these reserves are depleted, fat breakdown occurs in the liver (after fat gets released and transported there). This is composed of a large number of different steps, mediated and regulated by a large number of enzymes (like nearly all biochemical processes in your body). In the process, di- and triacylglycerols are broken down into glycerol and fatty acids (acyl groups) usually attached to coenzyme A (CoA). Glycerol gets phosphorylated and is one of the precursors of gluconeogenesis (de novo synthesis of glucose molecules). Long acyl-CoA molecules get "chopped down" commonly through beta-oxidation into small units - acetyl-CoA molecules which are really important. They are converted in the liver to compounds known as ketone bodies.

As you get many of acetyl-CoA molecules compared to a single glycerol molecule per one triglyceride (and two are needed for one glucose molecule), these are now a big deal. Luckily, the brain can indeed utilise these ketone bodies - upon entering the brain's cells, they're converted back into acetyl-CoA and used in the citric acid aka Krebs cycle to produce ATP - energy for the cells.

Usually, carbohydrates are broken down to acetyl-CoA, and when you eat them in abundance, acetyl-CoA doesn't get used for energy production, but gets chained into long acyl-CoA molecules in the liver, which are commonly bound into triacylglycerols (triglycerides) and stored in fat globules to be shipped off to adipocytes (fat cells).

As I mentioned, all of these processes are composed from a lot of steps, almost all of which are mediated by enzymes, and a lot of the steps are sites for regulation by various signals usually in the form of hormones. Cortisol is one of these. It stimulates the aforementioned storage of acetyl-CoA molecules, that is, fat production, and inhibits fat breakdown. As is the case with diseases, this breaks the entire mechanism so your body could have a great need to break down fat, but the excess cortisol's inhibition still overpowers the need, so very little fat gets broken down. Your cells therefore don't get these alternative sources of energy so they can hardly function in these conditions - leading to fatigue and weakness.

These reactions, their respective enzymes and the regulationof it all has a lot to do with thermodynamics, but, as you can see, hardly in the way your comment describes. This is all very, very simplified, but hopefully I've exposed enough of the underlying biochemistry for you to understand that it is possible for a person to be fat due to a disease, and not simply from overeating.

Christ, I never thought I'd be revising biochemistry on a Game of Thrones subreddit of all places.

Source: Harper's Illustrated Biochemistry, 28th Edition