Relative contribution of nervous system and hormones to hyperglycemia induced by thyrotropin-releasing hormone in fed rats

Toshiaki Ishiguro, Akihisa Iguchi, Yasuo Kunoh, Minehiro Goto, Kazumasa Uemura, Hisayuki Miura, Katsunori Noiwgaki, Nobuo Sakamoto

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13 Citations (Scopus)


In a continuation of our studies on the mechanism of central nervous system induced hyperglycemia in the rat, we evaluated the relative contribution of a direct neural effect on the liver and of certain hormones to the hyperglycemia induced by administration of thyrotropin-releasing hormone (TRH). The findings were compared with those of a previous investigation using neostigmine or 2-deoxy-D-glucose. In the present study TRH was injected into the third cerebral ventricle of rats, and the concentrations of hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine, were measured. Four groups of animals were evaluated: (1) intact rats; (2) rats receiving an infusion of somatostatin with insulin via the femoral vein to inhibit glucagon secretion and to maintain the basal insulin level; (3) rats bilaterally adrenalectomized (ADX) to prevent epinephrine secretion, and (4) ADX rats administered an infusion of somatostatin and insulin. Evaluation of the areas under the glucose curves for the rats receiving somatostatin with insulin, ADX rats, and ADX rats receiving somatostatin with insulin showed values 202, 50, and 79% of those observed in intact animals. These observations suggest that TRH-induced hyperglycemia results from at least two effects: a direct neural effect on the liver including a suppressive effect of epinephrine on insulin secretion (contributing about 79% to the total hyperglycemic effect) and a direct effect of epinephrine on the liver (contributing about 21% to the total hyperglycemic effect). The response of the intact rats was approximately 50% of that seen in rats given an infusion of somatostatin with insulin, suggesting that the parasympathetic outflow affecting insulin secretion or other factors acted to suppress the total hyperglycemia in intact rats. This pattern differs qualitatively from that observed previously with neostigmine or 2-deoxy-Z)-glucose. These findings do not rule out the contribution of other humoral or neuroactive substances released directly from brain or peripheral nerves that might influence hepatic glucose secretion.

Original languageEnglish
Pages (from-to)1-6
Number of pages6
Issue number1
Publication statusPublished - 1991


  • Brain
  • Epinephrine
  • Glucagon
  • Glucose
  • Insulin
  • Thyrotropin-releasing hormone


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