Theory of the "empty stomach" (peripheral)
This concept, proposed by Carlson, explains the sensation of hunger through signals from gastric mechanoreceptors. It was hypothesized that when food is evacuated, periodic motor contractions ("hunger motility") begin, which subsequently trigger the need for food.
However, this theory was deemed untenable for several reasons:
- S.V. Anichkov's autoexperiments demonstrated that the feeling of hunger does not strictly coincide with bouts of motility and can occur even when the stomach is at rest.
- Surgical practice confirms that individuals with a total gastrectomy still experience hunger when deprived of food.
- Experiments on dogs with deafferentation (transection of the vagus nerves and spinal cord) demonstrated that even with a complete loss of sensitivity in the gastrointestinal organs, the animals retained the drive to eat.
Theory of "hungry blood" (humoral)
Developed by I.P. Pavlov after the empty stomach theory came under criticism. The essence is that hunger arises due to changes in the chemical composition of the blood, specifically a decrease in nutrient levels.
Experimental evidence:
- The administration of glucose to hungry animals stopped feeding if the dose covered their carbohydrate requirement.
- Conversely, the administration of insulin, which lowers blood sugar levels, provoked eating even in satiated animals.
It was later established that the decisive factor is not the absolute glucose level itself, but its arteriovenous difference. When this difference approaches zero, the sensation of hunger is formed, which incidentally coincides with the onset of gastric "hunger" motility.
Critique of the humoral theory and twin experiments
Despite the logic of the humoral theory, it also turned out to be incomplete. Initially, it was believed that the blood contained specific hunger and satiety factors.
Refutation came through observations of conjoined twins who shared a common blood circulation but had separate nervous systems. When one girl was fed, her blood (and her sister's blood) became enriched with nutrients. However, the second girl did not experience a feeling of satiety—she continued to want to eat. This proved that nutrients in the blood alone are insufficient to generate satiety; a nervous component is strictly required.
Role of afferentation and anastomosis experiments
To prove the importance of impulses from the gastrointestinal tract to the nervous system, P.K. Anokhin conducted experiments with heterogeneous nerve anastomoses.
- Anastomosis with a somatic nerve. The vagus nerve (n. vagus) was anastomosed with the median nerve. In hungry animals, the electrical activity of the forelimb muscles increased during contractions of the empty stomach, dropped at rest, and became minimal after eating.
- Anastomosis with an autonomic nerve. When the vagus nerve was anastomosed with the chorda tympani, the salivation of the submandibular gland began to reflect the activity of the vagal nucleus: it increased during contractions of the empty stomach and sharply decreased after eating.
Direct electrophysiological recording also showed that the empty stomach generates high-amplitude impulses in the afferent fibers of the vagus nerve, which are suppressed upon the intake of food. This confirmed that tonic contractions of the walls of the empty stomach continuously send signals to the vagal nuclei, playing a role in the formation of hunger.
Briefly: answers to topical questions
Where are the main structures of the feeding center regulating hunger and satiety localized?
The main structures of the feeding center that regulate hunger and satiety are localized in the hypothalamus and medulla oblongata.
- Hunger center — located in the lateral hypothalamus; perceives signals of nutritional need and forms the motivation for food intake.
- Satiety center — located in the ventromedial nuclei of the hypothalamus and maintains reciprocal connections with the hunger center.
- Nuclei of the vagus nerve (n. vagus) — localized in the medulla oblongata; their functional activity increases upon receiving afferent impulses from contracting empty stomachs.
Which hormones and gastrointestinal peptides regulate the sense of hunger and satiety?
The sense of hunger and satiety is regulated by a number of gastrointestinal hormones and peptides that perform signaling functions.
- Ghrelin — synthesized in the stomach and intestines, directly stimulates appetite.
- Pentagastrin and motilin — signal the need for nutrients.
- Cholecystokinin — participates in satiety mechanisms and initiates the feeling of satiety.
- Somatostatin — also involved in satiety mechanisms.
- Neurotensin — initiates the feeling of satiety.
- Bombesin — signals the need for nutrients and is also capable of initiating the feeling of satiety.
Class and exam questions
What is the essence of the glucostatic mechanism?
The sensation of hunger arises when the difference in glucose content between arterial and venous blood (arteriovenous difference) approaches zero.
Why is the "empty stomach" theory considered untenable?
Because the sensation of hunger persists in patients after a total gastrectomy and in animals following complete gastrointestinal deafferentation.
What did observations of conjoined twins prove?
They proved that the presence of nutrients in the blood alone is insufficient for the feeling of satiety; the functioning of the nervous system (afferent signals from the gastrointestinal tract) is necessary.
What else to study on this topic
- Mechanisms of appetite and satiety formation
- Central mechanisms regulating eating behavior
- The role of the hypothalamus in the formation of the sensation of hunger
- Specific gastrointestinal receptors
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