Choosing snacks that have high water content, are airy, high in fiber and protein causes stronger satiety signals making the time between meals longer.

Signals arising from the long-term nutrient reservoir of the body may alter the sensitivity of the brain to hunger signals or short-term satiety signals.

The shimmering hope is that, if a faulty satiety signal triggers obesity, scientists may be able to administer the missing satiety protein to patients, much as diabetes is treated with insulin injections.

It seems likely that responses to incoming glucose during digestion play a role in the incretin amplification of insulin secretion during a meal, or in the generation of satiety signals from gut to brain.

Both insulin and leptin normally function as satiety signals to the hypothalamus in the brain; however, insulin/leptin resistance may reduce this signal and therefore allow continued overfeeding despite large body fat stores.

Scientists postulated that the obese mouse lacked a normal blood-borne satiety signal and that through the grafting it was receiving the missing protein.

The intestines also contain receptors that send satiety signals to the brain.

Long-term satiety signals from adipose tissue regulates short-term satiety signals.

After chyme is passed into the duodenum, signaling hormones such as cholecystokinin and leptin are released, causing reduction in gastric emptying and transmission of satiety signals to the hypothalamus.

Cannabinoid activity is reduced through the satiety signals induced by leptin release.