Satiety (physiology)

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With the feeling of satiety , the body signals that enough food has been taken in and that the meal can be finished. The feeling of being full arises in the brain . The mechanism of satiety is a very complex physical process involving numerous factors, all of which have still not been explored. Basically, hunger and satiety serve to regulate human food intake and to ensure that the organism is adequately supplied.

In addition to other physical processes, the hypothalamus in the diencephalon also controls the development of feelings of hunger and satiety. In this region of the brain, all external and internal stimuli and signals are processed during food intake and the production of neurotransmitters is triggered, which ultimately convey to the body that satiety has occurred. A distinction is made between the state of satiety ; this is only reached some time after the meal has ended and describes the phase until feelings of hunger reappear.

Physiological processes

It is considered certain that there is a satiety center in the ventromedial hypothalamus (VMH) and a hunger center in the lateral hypothalamus (LH) ; both centers are never active at the same time. However, research has not confirmed the assumption that the centers inhibit each other's activity. Rather, they both belong to the so-called Orexic network , which controls food intake. The first impulses of satiety when eating come from the stomach . As soon as the stomach wall expands due to the ingested food, this stimulus is reported to the hypothalamus by mechanoreceptors. However, filling the stomach alone does not trigger a saturation signal, as is now known. Chemoreceptors simultaneously register how many nutrients are ingested with food and also report this. Chemoreceptors are located in the intestines and in the liver . These signals together influence the acute feeling of hunger and thus the amount of food consumed. If only a large amount of low-calorie liquid is ingested, the stomach expands, but the chemoreceptors do not respond, so the feeling of satiety remains. This is also the case when a small amount of very high-energy food is consumed, which would cover the current energy requirement, but not stretch the stomach sufficiently. This fact favors the development of obesity with the preference for very high calorie foods. Studies have shown that proteins are slightly more satiating than carbohydrates and significantly better than fats .

When digestion begins, several hormones are formed in the intestine , some of which send further satiety signals to the brain via nerve tracts and some via the blood . The release of insulin plays a role, among other things, as do the hormones cholecystokinin and leptin, as well as the glucose concentration in the blood. As soon as a large number of satiety stimuli arrive in the hypothalamus, it in turn reacts with the release of appetite suppressing substances, including serotonin . It is still unknown how many factors are actually involved in the satiety mechanism; some hormones may not even be known.

The hormone leptin is released by the fat cells , and this is done continuously, not just when you eat. The more fat cells there are and the larger the stored fat reserves, the higher the leptin concentration in the blood. In 1994, researchers found in animal experiments with mice that this hormone has a decisive influence on the development of feelings of hunger and thus the interval between meals, but also the amount of food consumed. If the fat stores are well-filled, it basically has a hunger-suppressing effect. It is now clear, however, that leptin is not the decisive factor in the regulation mechanism of hunger and satiety. A genetic deficiency in leptin causes constant hunger, but an excess in the blood does not act as an appetite suppressant.

Current state of research


Various explanatory models exist to explain the control mechanism of hunger and satiety, which were originally developed as competing theories, but are now viewed as complementary explanations. The best known are the two-center theory , the thermostatic theory, the glycostatic theory and the lipostatic approach. The research is still ongoing. The theory of the existence of a hunger center and a satiety center in the hypothalamus was proposed in the 1940s. The existence of these centers is now widely recognized, but their importance is not as critical as originally thought.

In 1948 the thesis was put forward that food intake primarily depends on the organism's heat requirements. The body reacts to external temperature changes with changes in metabolism in order to regulate the body temperature . When it is cold, the energy requirement increases, when it is hot it decreases. In the so-called glucostatic theory (Mayer, 1953) it is assumed that biochemical changes in the blood signal hunger and satiety. Then a drop in the insulin level triggers feelings of hunger, and the release of the hormone signals satiety. The insulin level corresponds to a high or low glucose concentration in the blood, but it can also be severely impaired by pure amino acid complexes. There are glucose sensors in the hypothalamus, in the brain stem and in the liver. Insulin also increases serotonin output in the brain, which also leads to satiety signals.

In the lipostatic theory (Kennedy, 1953) the hormone leptin , which is produced in adipose tissue , plays an essential role . The better the fat cells are filled, the more leptin there is in the blood. It is considered to be a long-term regulator of feelings of hunger, which mainly influences the intervals between meals. It is also referred to in the specialist literature as the obesity signal . For a long time it was assumed that obesity was caused by a leptin deficiency because such a genetic defect caused mice to overeat in animal experiments, but this thesis has now been refuted. In fact, there is a lot of leptin in the blood of overweight people without this high concentration having an anti-hunger effect. According to the current state of research, it is assumed that a leptin deficiency leads to increased feelings of hunger in order to protect the body from a deficiency, but that an excess of leptin does not have any adverse effects. Leptin administration to obese people did not lead to any significant weight loss in studies.

In the selfish brain theory , stress plays a central role. The brain primarily ensures its own energy supply. Under stress, depending on the reactivity of the stress system, stress hormones are released and the insulin concentration in the blood is lowered or an incentive to eat is set.

In the past few years, several hormones have been discovered that play a role in satiety. One of these is cholecystokinin , which is produced in the intestine and mainly promotes the emptying of the gallbladder and the production of enzymes by the pancreas . But there are also receptors in the hypothalamus for this hormone, which stimulates the release of serotonin there. A protein called mTOR , in conjunction with the amino acid leucine, is said to be involved in the development of feelings of hunger. In rats, a high mTOR concentration in the brain led to a rapidly decreasing food intake, and a deficiency to permanent eating.

In 2005, the appetite-suppressing and satiety-promoting effects of the hormone oxyntomodulin , which is formed in the small intestine during digestion , were demonstrated in a controlled study. Participants were injected with the hormone 30 minutes prior to eating. The result was confirmed in another study in 2006. On average, the subjects consumed 17 percent less energy from food (see: physiological calorific value ).

According to an American study, a protein-rich diet (30% of nutritional energy from proteins, 50% carbohydrates, 20% fat) leads to a stronger and longer-lasting satiety effect than a diet with the protein content of a maximum of 15 percent recommended by most nutritionists. Saturation was achieved despite gradually decreasing leptin release and increasing ghrelin levels , with ghrelin being an important trigger of feelings of hunger. It is controversial whether an increased protein content, as in low-carb diets, brings health risks.

Psychological influences

The research is still not completed, possible psychological influences are not taken into account in most studies, as there are hardly any interdisciplinary projects. Nutritional psychology tries to close this gap . For example, some substances that suppressed feelings of hunger in animal experiments turned out to be almost ineffective in studies with test persons. One explanation for this is that the eating behavior of mice or rats is hardly influenced by the psyche.

In humans, on the other hand, psychological as well as physiological factors seem to play an important role in conveying a feeling of satiety. In 2005 , researchers at Cornell University in Ithaca (USA) discovered that visual impressions determine the feeling of satiety even more than the actual stomach filling: A person usually eats - regardless of the amount of calories actually consumed and the portion size - until the Plate visibly emptied. She neither feels overly saturated after larger servings nor is she aware of the higher calorie intake.

Nutritional psychologists have also found that the food supply, appetite and palatability of food can have a strong influence on the amount eaten and lead to the ignoring of satiety signals. A well-stocked buffet with a large selection of dishes is generally tempting due to the external incentive to overeat. Increased food intake due to good taste could even be observed in animal experiments with rats, who ate significantly more from a so-called “cafeteria diet” with a lot of sugar and fat than is usual and necessary. In addition, eating behavior in society is influenced by that of the people sitting next to you. In tests, test persons ate not only "good eaters" up to 25 percent more than usual.

Disorders of the satiety mechanism

Both in obesity and in eating disorders such as bulimia and binge eating (food cravings), the regulatory mechanism consisting of appetite, hunger and satiety does not work or does not work well. The causes of this disorder have not yet been fully researched, although here again several factors can play a role. It has been proven that when the stomach is enlarged from frequent large portions, the mechanoreceptors react later because it takes longer for the stomach wall to stretch. For hasty eaters, the meal is sometimes over before the brain can send the first satiety signals.

It is unclear whether obese people no longer produce clear satiety stimuli or whether they do not perceive them. Some researchers believe that repeated diets disrupt the metabolism and thus the regulatory system for hunger and satiety. The body no longer gives signals to finish a meal, since it assumes that it has to build up reserves for future periods of hunger (diet). The theory that “food addiction” is actually an addiction is controversial as some requirements for this definition are not met. However, high-calorie foods trigger, among other things, the release of the hormone dopamine , which is also the case when consuming intoxicants. An emotional eating disorder can also lead to impaired appetite, hunger and satiety. These are deeper feelings such as sadness, fear, tension or anger that unbalance the hunger-satiety system.

In the case of cravings, which occur regularly in some overweight people as well as in bulimia and binge eating, control over food intake is completely lost. It only ends when all the food available has been consumed or when you feel sick. There are several theories as to what causes these binge eating. Nutritional psychologists see so-called restrictive or restrained eating behavior as a strong risk factor. This refers to both regular dieting and constant discipline when eating. Restrained eaters usually end a meal "head-controlled" before they feel full , in order to maintain their weight and avoid "unhealthy" foods. As a result, the diet is often permanently low in calories. Psychologists assume that the body defends itself against this restrictive eating behavior with periodic cravings as soon as the will control becomes weaker under stress or a certain occasion. This cravings is also often observed after diets, so that weight loss is usually more than offset by the so-called yo-yo effect .

In people with Prader-Willi syndrome , this leads to an excessive, compulsive feeling of hunger, which has physical causes and cannot be consciously regulated.

Satiety agents

In the treatment of obesity , various methods are used to limit the amount of food consumed by those affected.

In extreme cases, a gastric band or balloon is inserted into the stomach to artificially make it smaller again. As a result, the portion size per meal is severely limited by a feeling of fullness and mechanical satiety stimuli.

Dietary fibers with a high water-binding capacity, such as glucomannans (konjac) or psyllium husks , have a moderate effect, although they only affect the pressure receptors of the gastric mucosa , but not its chemoreceptors, so that their effect disappears again when the stomach is emptied. Some preparations (mostly medical products in capsule form) are said to have a similar effect, but the effect is individually dose-dependent and is only noticeable to a limited extent in very overweight people who hardly eat because of feelings of hunger. While many of these drugs remain over-the-counter, some have become prescription- only after bowel obstruction as a result of their use .

There are also various appetite suppressants on the market that affect either the hunger center or the satiety center in the hypothalamus. This is mostly achieved by stimulating the production of norepinephrine , dopamine and serotonin in the brain. Activation of the serotonin receptor subtype 2C (5-HT 2C ) is also discussed as a mechanism of the anorectic effect of classic appetite suppressants. Inhibition of the cannabinoid receptor CB 1 also leads to a significant inhibition of appetite. Studies have shown that the effects of these agents on the brain wear off significantly after a few weeks. In the 1960s, amphetamine derivatives in particular were used as appetite suppressants that act on the central nervous system . Most of these preparations are no longer approved, as prolonged use leads to dependence and can trigger serious side effects. Most drugs of this type are no longer marketable in Europe and the USA and can only be obtained via the Internet.

Side dishes

Foods rich in carbohydrates such as pasta , potatoes , dumplings, etc. are used as “side dishes” in gastronomy . Like. Denotes, which are supposed to provide energy and fiber during a meal in order to contribute to satiety. The same applies to the various, mostly heavily sweetened desserts , which at the end of a multi-course menu colloquially “close the stomach”, that is, to trigger the insulin-induced feeling of satiety.

Web links

Individual evidence

  1. a b c d e DGE: Molecules regulate weight (2002)
  2. a b Susanne Klaus: Regulation of hunger and satiety. 2005
  3. Etiological factors that lead to increased energy intake ( Memento from April 16, 2013 in the Internet Archive )
  4. Nutritional review : How does the feeling of satiety arise? (2002) ( Memento of the original from September 27, 2007 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. @1@ 2Template: Webachiv / IABot /
  5. Focus report: Appetite brake in the brain (2006)
  6. Small intestine hormone suppresses appetite and increases energy expenditure ( Memento from December 24, 2011 in the Internet Archive )
  7. Forum Nutrition
  8. Focus report: Waiting for the miracle pill (2006)
  9. Obesity Research, 2005, Vol. 13, p. 93
  10. Michael Boschmann: Mechanisms for the regulation of hunger and satiety, p. 20f. ( Memento of the original from September 30, 2007 in the Internet Archive ) Info: The archive link was automatically inserted and not yet checked. Please check the original and archive link according to the instructions and then remove this notice. @1@ 2Template: Webachiv / IABot /
  11. Quarks & Co: The most important rules for the wolverine
  12. Why diets make you fat ( Memento from January 13, 2007 in the Internet Archive )
  13. a b Rolf Degen: The high from gluttony. In: Tabula 01/2002
  14. DGE: Food and Psyche
  15. Changed prescribing rules for CM3 capsules in Pharmazeutische Zeitung online
  16. Consumer advice center Baden-Württemberg: Appetite suppressant  ( page can no longer be accessed , search in web archivesInfo: The link was automatically marked as defective. Please check the link according to the instructions and then remove this notice. (PDF; 75 kB)@1@ 2Template: Toter Link /  
  17. Dangerous slimming products ( Memento from February 12, 2013 in the web archive )