Leptin
The satiety hormone released by fat tissue to signal energy stores to the brain.
Leptin is a hormone released by fat tissue in rough proportion to how much of it you have. It reports long term energy stores to the brain, where it acts on the hypothalamus to influence appetite, energy expenditure and reproductive function.
It was discovered in mice that became enormously obese because they could not make it, and giving it back normalised them. That result led to an obvious expectation, that leptin would treat human obesity, and it did not. Almost everyone with obesity has high leptin already; the brain is not listening well, a state usually described as leptin resistance.
Where it matters practically is dieting. As body fat falls, leptin falls with it, and it falls faster than fat does. The brain reads that as a shortage and responds sensibly for a species evolved around famine: hunger rises, spontaneous movement declines, and thyroid and reproductive signalling dial down.
That is a mechanism behind metabolic adaptation, and it reframes the difficulty of maintaining weight loss as physiology rather than weakness. The signal is doing exactly what it evolved to do.
Sleep moves it in the wrong direction. Short sleep is associated with lower leptin and higher ghrelin, which is a plausible route by which poor sleep makes appetite harder to manage.
There is nothing to buy here. Leptin is a protein, so swallowing it would digest it, and products marketed as leptin boosters or leptin resistance cures have no meaningful evidence behind them. What genuinely raises leptin is having more fat, which is not the goal.
In practice, expect appetite to rise as a diet progresses, plan periods at maintenance rather than an endless push, protect sleep, and use our calorie deficit calculator to keep the deficit moderate enough to live with.