Ghrelin is a hormone produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas that stimulates hunger. Ghrelin levels increase before meals and decrease after meals. It is considered the counterpart of the hormone leptin, produced by adipose tissue, which induces satiation when present at higher levels. In some bariatric procedures, the level of ghrelin is reduced in patients, thus causing satiation before it would normally occur.
Leptin is a 16 kDa protein hormone that plays a key role in regulating energy intake and energy expenditure, including appetite and metabolism. It is one of the most important adipose derived hormones. The ''Ob(Lep)'' gene (Ob for obese, Lep for leptin) is located on chromosome 7 in humans.
The effects of leptin were observed by studying mutant obese mice that arose at random within a mouse colony at the Jackson Laboratory in 1950. These mice were massively obese and excessively voracious. [...]
Leptin and ghrelin seem to be the big players in regulating appetite, which consequently influences body weight/fat. When we get hungrier, we tend to eat more. When we eat more, obviously, we maintain our body weight or gain that weight back.
Both leptin and ghrelin are peripheral signals with central effects. In other words, they’re secreted in other parts of the body (peripheral) but affect our brain (central).
Leptin is secreted primarily in fat cells, as well as the stomach, heart, placenta, and skeletal muscle. Leptin decreases hunger.
Ghrelin is secreted primarily in the lining of the stomach. Ghrelin increases hunger.
Both hormones respond to how well-fed you are; leptin usually also correlates to fat mass — the more fat you have, the more leptin you produce. Both hormones activate your hypothalamus (a part of your brain about the size of an almond).
And here’s an important point: both hormones and their signals get messed up with obesity.