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肾上腺素刺激前后胰腺外胰高血糖素和胰高血糖素样免疫反应性的色谱模式以及胰高血糖素在肾上腺素诱导的肝脏葡萄糖过度生成中的作用。

Chromatographic pattern of extrapancreatic glucagon and glucagon-like immunoreactivity before and during stimulation by epinephrine and participation of glucagon in epinephrine-induced hepatic glucose overproduction.

作者信息

Lickley H L, Kemmer F W, Gray D E, Kovacevic N, Hatton T W, Perez G, Vranic M

出版信息

Surgery. 1981 Aug;90(2):186-94.

PMID:6114573
Abstract

To characterize the glucagon released in response to epineephrine in depancreatized dogs, plasma samples before and during epinephrine infusion were subjected to molecular-sieve chromatography on Bio-Gel P-30 columns. The chromatographic profile for extrapancreatic immunoreactive glucagon (eIRG) revealed two glucagon moieties of molecular weight 9,000 to 12,000. GLI of this molecular weight was released in response to epinephrine only under conditions of prevailing hyperglycemia. To determine if glucagon's participation in epinephrine-induced hepatic glucose overproduction in diabetes was dependent upon the degree of metabolic control, six conscious depancreatized dogs were infused with epinephrine or epinphrine plus somatostatin, under conditions of prevailing hyperglycemia or normoglycemia. Under normoglycemic conditions, epinephrine stimulated eIRG release, but there was a similar rise in hepatic glucose production (Ra) with or without glucagon suppression by somatostatin. Under hyperglycemic conditions, epinephrine stimulated eIRG and GLI release, and the rise in Ra was significantly greater with epinephrine than with epinephrine plus somatostatin infusion. Thus, under conditions of good metabolic control, epinephrine increased hepatic glucose production independently of glucagon, whereas with poor metabolic control, glucagon contributed to hepatic overproduction of glucose.

摘要

为了描述去胰腺狗体内肾上腺素刺激释放的胰高血糖素的特征,在输注肾上腺素前及输注过程中采集的血浆样本,通过Bio-Gel P-30柱进行分子筛色谱分析。胰腺外免疫反应性胰高血糖素(eIRG)的色谱图显示有两个分子量为9000至12000的胰高血糖素部分。只有在持续高血糖的情况下,这种分子量的胰高血糖素样免疫反应物(GLI)才会因肾上腺素刺激而释放。为了确定糖尿病中胰高血糖素参与肾上腺素诱导的肝脏葡萄糖过度生成是否取决于代谢控制程度,对6只清醒的去胰腺狗在持续高血糖或血糖正常的情况下输注肾上腺素或肾上腺素加生长抑素。在血糖正常的情况下,肾上腺素刺激eIRG释放,但无论生长抑素是否抑制胰高血糖素,肝脏葡萄糖生成率(Ra)都有类似升高。在高血糖情况下,肾上腺素刺激eIRG和GLI释放,且肾上腺素组的Ra升高显著大于肾上腺素加生长抑素输注组。因此,在代谢控制良好的情况下,肾上腺素独立于胰高血糖素增加肝脏葡萄糖生成,而在代谢控制不佳时,胰高血糖素会导致肝脏葡萄糖过度生成。

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