Leptin is a satiety hormone (makes you feel full, or better yet a lack of hunger) that is opposed by the actions of ghrelin which is a hunger hormone. It wasn't even discovered until 1994 by Dr. Jeffrey Friedman, MD. In obesity, a decreased sensitivity to leptin occurs resulting in an inability to detect satiety despite high fat stores. You would think that because leptin is synthesized in fat cells, that excess body fat would lead to increased satiety. Going from 10% bodyfat to 18% bodyfat for instance would most likely increase satiety because you'll have more leptin production, but at a certain point on the road to obesity the body becomes less sensitive to leptin and many obese people feel hungry virtually all the time, which leads to more eating, less satiety, and a vicious cycle that is tough to reverse.

It is primarily produced in the adipocytes of white adipose tissue and circulates in blood in free form and bound to proteins. Blood levels of leptin are higher between midnight and early morning which suppresses appetite during the night.

Here are some things you should know about leptin:

Levels decrease after short term fasting of 24-72 hours even when changes in fat mass do not occur

Leptin plays a role in the adaptive response to starvation.

Leptin levels are decreased by sleep deprivation. You ever had a bad nights sleep and craved carbs the next day? This is why.

Leptin level is increased by insulin. You know how you eats a ton of carbs and get that nice full feeling? This is in part due to the insulin response from the carbs.

There have been cases of leptin deficiency found in severely obese children where their bodies did not produce adequate leptin or that there was sufficient amounts of leptin circulating in the bloodstream, but biologically inactive ineffective due to effective receptor binding.