Gastric Component and Reception
The initial stage of nutritional demand is linked to the physical state of the gastrointestinal tract. Following the evacuation of food, the stomach contracts, occupying a minimal volume while its walls thicken.
These anatomical changes lead to the irritation of mechanoreceptors within the organ wall. Simultaneously, chemoreceptors are activated, stimulated by the accumulation of gastric mucus and the so-called 'emptiness' factor. The resulting afferent impulse flow triggers a complex cascade of neurohumoral regulation.
Neurohumoral Pathway
Signals from empty stomach receptors are transmitted to the brain via the following chain:
- Excitation of the vagus nerve nuclei (n. vagus).
- Transmission of impulses to specialized neurons in the hypothalamus.
- Activation of anterior pituitary (adenohypophysis) cells via neurosecretory mechanisms (involving nerve growth factors, including insulin-like oligopeptides).
- Increased production of tropic hormones by the pituitary gland.
The primary effect of tropic hormones at this stage is the stimulation of nutrient deposition. Carbohydrates and lipids are actively stored from the bloodstream into the liver, skeletal muscle, and adipose tissue. Clinical observation shows that these processes occur significantly faster in individuals with excess body weight, worsening reserve accumulation.
Functional Systems Theory: Two Phases of Hunger
According to the theory of functional systems, neural centers receive information about nutritional needs through two successive factors:
First Phase (Gastric Afferentation): Develops as food is evacuated. At the level of the medulla oblongata, it triggers periodic 'hunger' motility. At the hypothalamic-pituitary level, a critical process occurs: the enhanced transfer of nutrients from the blood into storage depots. As a result, plasma nutrient levels decrease, setting the stage for the transition to the second phase, even if substantial bodily reserves remain.
Second Phase ('Hunger Blood'): Nutrient-depleted blood becomes saturated with informational molecules—oligopeptides (ghrelin, motilin, pentagastrin, oxytocin, neuropeptide Y). If these substances are experimentally administered to a fed animal, it will initiate food-seeking behavior.
Conscious Perception and Clinical Evidence
Mechanical impulses from the empty stomach are not subjectively perceived by a person on their own. Hunger is consciously recognized only when 'hunger blood' factors reach the limbic structures of the brain and activate them. Only then does the subject switch to food-seeking behavior.
This dual nature of hunger (afferentation + humoral factors) is supported by classic clinical examples:
- Gastrectomy: Patients without a stomach continue to experience hunger. The mechanical component is absent, but metabolic demand persists, leading to the formation of informational molecules in the bloodstream—the very essence of 'hunger blood'.
- Conjoined Twins: In cases of shared circulation, feeding one twin does not always quench the hunger of the other. The signaling from the hungry child's empty stomach is so powerful that it locally blocks the satiety-inducing effects of 'sated blood' factors coming from the well-fed twin.