Central thyrotropin-releasing hormone elicits systemic hypoglycemia in mice.
Thyrotropin-releasing hormone (TRH), injected into the central nervous system (CNS) in rats, has been shown to elicit systemic hyperglycemia. In the present study, central TRH administration significantly decreased the plasma glucose in mice. The hypoglycemic response could be blocked by pretreatment with the muscarinic cholinergic antagonist, atropine methyl bromide, or the diabetogenic beta-cytotoxin, alloxan, implicating the involvement of the parasympathetic system and insulin-secreting cells in the endocrine pancreas. The role of TRH in the CNS in the autonomic regulation of glucose homeostasis is discussed.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis*; D001921:Brain / Q000187:drug effects*; D007276:Injections, Intraventricular; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D051379:Mice; D010275:Parasympathetic Nervous System / Q000187:drug effects*; D011976:Receptors, Muscarinic / Q000187:drug effects; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*
D001786:Blood Glucose; D007328:Insulin; D011976:Receptors, Muscarinic; D013973:Thyrotropin-Releasing Hormone