Adrenal and liver participation in the rat's post-stress diabetic response.
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.
D000311:Adrenal Glands / Q000187:drug effects / Q000503:physiopathology*; D000315:Adrenalectomy; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D002746:Chlorpromazine / Q000494:pharmacology; D003920:Diabetes Mellitus / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D006029:Glycosuria; D006943:Hyperglycemia / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D010180:Pancreatectomy; D051381:Rats; D013312:Stress, Physiological / Q000150:complications / Q000503:physiopathology*
D001786:Blood Glucose; D001798:Blood Proteins; D002746:Chlorpromazine