Table of Contents
Page created on March 4, 2019. Not updated since.
Introduction
Food intake is regulated through the sensations of hunger, appetite and satiety. Appetite relates to hunger, but they are not the same. Hunger is the physical need for food that is related to your body’s need for nutrients. It cannot be controlled as it is instinctive. Ignoring hunger leads to low blood glucose. Satiety is opposite of hunger.
Appetite is the desire to eat. It is what you feel when you really want some chocolate or fries. Appetite can (and in most cases should) be ignored, as the food you eat just based on appetite is often food you don’t need.
After satiety has set in and you’re not really hungry anymore can appetite lead to further food intake. Changes in appetite play a large role in food intake. If you have a large appetite will your food intake be higher than normal and if you have a lack of appetite will the food intake be much lower than you need.
Regulating the food intake is important. This regulation is not only quantitative but also qualitative, i.e. it affects what types of nutrients you crave as well.
Afferent signals in the regulation of food intake
These signals are what the brain uses to determine how it should regulate the food intake. There are three major signals: the nutritional state, the feeding state and the body temperature.
The nutritional state is determined by the size of fat stores and the blood glucose. The level of leptin is proportional to the size of fat stores, and the level of insulin is proportional to the blood glucose. Central brain nuclei can check the levels of these hormones to determine the nutritional state. This signal provides a long-term influence on the regulation of food intake.
The feeding state determines the hunger and satiety. It’s signalled by both humoral and neural signals. Stretch of the GI tract provides neural signals through the vagus nerve, while GI peptides provide humoral signals by acting on receptors in the arcuate nucleus in the brain. For evoking satiety is GI stretch, high blood glucose and CCK the most important factors. Hunger is evoked by lack of GI stretch, by decreased blood glucose and by ghrelin. This system has a short-term influence on food intake.
The body temperature is the last signal. Acute cold exposure enhances food intake, while warm environment of high body temperature inhibits food intake.
Central regulation of food intake
The aforementioned neural and humoral signals reach the brain by acting through the brain stem, the nucleus of solitary tract, the dorsal nucleus of vagus nerve and the ventromedial nucleus of the hypothalamus. Indeed, the hypothalamus is regarded as the most important part of the CNS in regulating food intake.
Psychological factors from higher cortical areas are also important, as evidenced by the conditions anorexia nervosa and bulimia nervosa.
Many peptides act on the hypothalamus to regulate food intake. We separate them into orexigenic (feeding-promoting) and anorexigenic (feeding-inhibiting) peptides. Here are some of them:
| Orexigenic peptides | Anorexigenic peptides |
| Neuropeptide Y (NPY) | Cholecystokinin (CCK) |
| AgRP | Melanocortin (MSH) |
| Orexin | Corticotrophin releasing-hormine (CRH) |
| Ghrelin | Leptin |
| Cannabinoids (not peptides) | Insulin |
| Serotonin (not a peptide) |
Central NPY, AgRP and orexins are the most important orexigenic peptides. Leptin and insulin are signals of nutritional state from the periphery. CCK is a signal of satiety (feeding state) from the periphery.
Disorders of food intake
There are many disorders of food intake, however the mechanism of them is not well known. Changes to the afferent signals or central components may lead to hypophagia or hyperphagia and thereafter changes of body weight.
Anorexia nervosa is a condition in which a person misjudges their own body weight as too fat and therefore decreases their food intake. The causes are largely unknown but there are genetical, environmental, psychological and sociocultural elements involved. Anorexia is highly inheritable. A role of abnormalities in the gene for AgRP or its receptor has been determined.
Bulimia nervosa is a condition in which episodes of feeding leaves the person feeling guilting, after which they vomit. No clear cause is known but like for anorexia nervosa is the background multifactorial.
Recent research has shown that abnormal weight gain isn’t just due to a lack of willpower but also due to abnormalities of biological factors like hormones. Sedentary lifestyle of western countries and poor diet are major contributors, but recent research has determined that genetic factors may be involved in 40-70% of cases of obesity. These genetic factors mostly involve polymorphisms of genes that are involved in regulation of food intake.
Especially leptin has been implicated in this. Leptin resistance or leptin deficiency are implicated as mechanisms that may be important in development of obesity. As a person gets progressively more obese will the adipose tissue contain more fat, which stimulates the adipocytes to produce more leptin. As the leptin levels increase in the plasma should the hypothalamus understand that the body is more than sufficiently fed and therefore decrease food intake. This mechanism is deficient in obese people. There is currently no clinical application of this information, but there may be in the future.