Agarwala G C, Mishra R, Jaiswal G, Bapat V
Indian J Med Res. 1989 Oct;90:372-8.
Glucagon (0.01 microgram) administered through the intracerebroventricular route in anaesthetised mongrel dogs, caused a significant rise in blood glucose and a fall in liver glycogen (P less than 0.01). Concurrently, it increased the liver phosphorylase, glutamic oxaloacetic transaminase, glutamic pyruvic transminase and lipase activities by 30 min. Identical changes were observed in vagotomised animals. In pancreatectomised animals as well as in spinal cord transectomised animals, glucagon did not cause these changes. The study indicated that the hyperglycaemia produced by the centrally administered glucagon, is possibly a result of liver glycogenolysis and gluconeogenesis induced by endogenous glucagon secreted from the pancreas, the stimulus for which is the hypothalamo-pancreatic fibres responding to glucagon sensitive neurones in the hypothalamus.
在麻醉的杂种犬中，经脑室内途径给予胰高血糖素（0.01微克），可导致血糖显著升高和肝糖原减少（P＜0.01）。同时，它在30分钟内增加了肝磷酸化酶、谷草转氨酶、谷丙转氨酶和脂肪酶的活性。在迷走神经切断的动物中观察到了相同的变化。在胰腺切除的动物以及脊髓横断的动物中，胰高血糖素并未引起这些变化。该研究表明，中枢给予胰高血糖素所产生的高血糖，可能是胰腺分泌的内源性胰高血糖素诱导肝糖原分解和糖异生的结果，其刺激因素是下丘脑 - 胰腺纤维对下丘脑中胰高血糖素敏感神经元的反应。
