Why is the rat satiated? - briefly
Ingestion of a calorically sufficient meal stimulates gastrointestinal hormones such as cholecystokinin and leptin, activating hypothalamic satiety circuits and producing a state of fullness. Consequently, further feeding is inhibited until energy balance declines.
Why is the rat satiated? - in detail
Rats terminate feeding when physiological signals indicate sufficient energy intake. Gastric distension activates stretch receptors that transmit afferent signals to the nucleus of the solitary tract, producing an immediate inhibition of licking behavior. Simultaneously, the presence of nutrients in the small intestine triggers the release of cholecystokinin (CCK) and peptide YY, which act on vagal afferents and hypothalamic nuclei to reinforce satiety. Elevated plasma glucose stimulates insulin secretion, which crosses the blood‑brain barrier and suppresses orexigenic neurons in the arcuate nucleus while enhancing activity of pro‑opiomelanocortin (POM POMC) cells. Leptin, released from adipose tissue, provides a longer‑term indication of energy stores, reducing the firing rate of neuropeptide Y (NPY) neurons and sustaining the satiated state.
Key mechanisms can be grouped as follows:
- Mechanical feedback from stomach expansion
- Hormonal responses to intestinal nutrients (CCK, peptide YY, glucagon‑like peptide‑1)
- Glycemic and insulin signals reflecting post‑prandial glucose rise
- Adiposity signals (leptin) modulating hypothalamic circuits
- Central integration in the hypothalamus and brainstem that suppresses feeding motor output
Experimental data show that pharmacological blockade of CCK receptors or vagotomy markedly increases meal size, confirming the necessity of gut‑derived signals. Genetic models lacking leptin or its receptor display persistent hyperphagia despite normal gastric feedback, indicating that peripheral and central cues operate in concert.
Overall, satiation in rats results from a multilayered feedback system that combines immediate mechanical cues, rapid hormonal responses to ingested nutrients, and longer‑term adiposity signals, all converging on hypothalamic pathways that inhibit further food intake.