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                <term xml:lang="en">food intake</term>
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              <p>&lt;div&gt;&lt;p&gt;Severe calorie restriction in mouse models has highlighted the crucial role of the ghrelin system in maintaining glycemia and promoting survival. We hypothesized that if ghrelin acts as a survival signal, enhancing the responsivity of the GH secretagogue receptor (GHSR) should favor GHSR protective responses. To test this, we used rats with genetically enhanced GHSR sensitivity (Ghsr Q343X ) and wild-type littermate controls and examined their acute responses to pharmacological challenges. Consistent with our hypothesis, Ghsr Q343X rats, despite normal glucose and insulin tolerance, exhibited a significant increase in blood glucose in response to GHSR agonism, accompanied by elevated counter-regulatory hormones including corticosterone.&lt;/p&gt;&lt;p&gt;Concurrently, these rats displayed a notable decrease in locomotor activity and delayed feeding response. Also, GHSR agonism partially altered the cocaine-induced hyperlocomotion of Ghsr Q343X rats while they showed unaltered locomotor sensitization to cocaine. At the cellular level, functional studies indicated that the Ghsr Q343X mutation prolongs ghrelin-induced GHSR-G protein canonical signaling. Altogether, in a model of increased GHSR sensitivity, GHSR agonist stimulation was sufficient to promote a robust blood glucose increase, while the acute feeding response was delayed in a context of unexpected hypolocomotor response. This mechanism may have implications for severe states of undernutrition such as restrictive anorexia nervosa.&lt;/p&gt;&lt;/div&gt;</p>
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