AI Article Synopsis
- The study shows that exposure to restraint stress, alongside chlorpromazine, leads to a temporary increase in blood sugar levels (post-stress diabetic response) in both normal and adrenalectomized rats.
- This response was linked to a hormone (alpha2-inhibitor) that reduces glucose absorption in tissues, indicating it is produced in the liver due to somatotrophic hormone (STH) stimulation without needing glucocorticoids.
- Although adrenalectomized rats experienced lower overall blood sugar levels after stress compared to controls, their glucose production still increased, suggesting that even without adrenal glands, stress can trigger glucose production in the body.
Article Abstract
Sixty minutes of restraint stress, preceded by chlorpromazine administration which stimulates somatotrophic hormone secretion (STH), produced an acute post-stress diabetic response (PDR) in normal-intact rats as well as in adrenalectomized rats. This PDR lasted 3 to 4 hours and was evaluated by glucemia and glucosuria determination and by the appearance of an insulin antagonist, alpha2-glycoprotein STH-dependent, called alpha2-inhibitor, which inhibits glucose uptake by isolated tissues. When tested in the suprahepatic blood of animals after stress it showed increased activity, both in normal and in adrenalectomized rats. This result permits us to state that alpha2-inhibitor may be produced in the liver by and action of STH and without primary glucocorticoid participation. The post-stress hyperglucemic response of adrenalectomized rats had a similar tendency to that of the control, although with initial and final values of glucemia significantly below the control. This response supports the diea that postadrenalectomy gluconeogenesis was evoked during and after the systemic stress.
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| http://dx.doi.org/10.1055/s-0028-1093619 | DOI Listing |
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