Satiety is the state of satisfaction after consuming food. It is the inhibitory response that stops a person from consuming more food after he or she is full. It is one of the necessary controls for maintaining homeostasis in many organisms. The limbic region and the cerebral cortex are the main structures of the central nervous system responsible for the regulation of satiety (Ahima & Antwi, 2008). As more research emerges in this field, it is becoming apparent that many peripheral organs play an integral role in communicating with the brain regarding a person’s satiety.
History and Function
Eating is necessary for survival. It is the most efficient way of providing the body with all the calories and nutrients required for optimal function. Food is broken down into small molecules that drive metabolism. Some food is processed and used immediately, while other food goes into storage as fat. The brain is responsible for monitoring energy expelled by daily activities as well as signaling hunger when supplies of energy are quickly being depleted. Food has rewarding qualities that consequently increase appetite beyond metabolic needs (Ahima & Antwi, 2008). Hypotheses on peripheral satiety signals have been proposed since the 1960s (Sharkey, 2009). It was thought that biomolecules such as glucose and fat could trigger a signal that would alert the brain whenever enough food had been consumed to meet metabolic needs. Since then, the discoveries of leptin and leptin receptors have been key in studying how satiety is regulated.
Anatomy and Physiology
Currently, neuronal and hormonal signals from the gastrointestinal tract are thought to control satiety (Ahima & Antwi, 2008). As food is consumed, the gastrointestinal tract will send signals to the central nervous system. The nucleus tractus solitarii (NTS) is a cluster of nerves that run through the medulla oblongata. These nerves will project these signals to the visceral sensory thalamus (part of the limbic system), which will then relay the information to the visceral sensory cortex (Ahima & Antwi, 2008). The visceral sensory cortex is part of the cerebral cortex. It is the structure that facilitates the perception of gastrointestinal satiety.
Leptin is a primary hormonal signal that controls satiety. It is a hormone secreted by adipocytes in the adipose tissue, also known as fat. Leptin levels directly correlate to fat levels in the body. This hormone is thought to be the long-term control of energy homeostasis whereas insulin has been shown to only have a short-term effect on satiety and energy homeostasis. Higher leptin levels mean that a lot of adipose tissue is present. There are two types of leptin receptors: short leptin receptors and long leptin receptors. Short leptin receptors are not extensively studied, but are thought to help the hormone cross the brain capillaries (Ahima & Antwi, 2008). Long leptin receptors are located in several regions of the brain, including the hypothalamus, the brainstem, and the regions of the brain that control feeding and energy outflow (Ahima & Antwi, 2008). High leptin levels will decrease appetite and increase energy expenditure whereas low leptin levels will decrease energy expenditure and increase appetite. In other words, high leptin levels will increase satiety.
Disease and Disorder
Lack of satiety results in many health problems including obesity, diabetes, and depression. Current studies in obesity indicate findings relating overeating with possible leptin resistance. Resistance to leptin will cause leptin levels to be high without the body realizing it. Satiety is not achieved in this case, which will keep appetite from decreasing. Leptin levels will undergo a net increase in these individuals if voluntary controls are not used to stop eating.
Overabundance of satiety can also result in health problems. Individuals with congenital leptin deficiency have low appetite due to the overactivity of brain regions associated with satiety (Ahima & Antwi, 2008).
See also: Ageusia; Dysgeusia; Hunger; Supertaster; Thirst
Ahima, Rexford S., & Daniel A. Antwi. (2008). Brain regulation of appetite and satiety. Endocrinology and Metabolism Clinics of North America, 37(4), 811—823. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2710609/
Murphy, Kevin G., & Stephen R. Bloom. (2006). Gut hormones and the regulation of energy homeostasis. Nature, 444, 854—859.
Sharkey, K. A. (2009). Peripheral satiety signals: View from the chair. International Journal of Obesity, 33, S3—S6. Retrieved from http://www.nature.com/ijo/journal/v33/n1s/full/ijo20098a.html