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葡萄糖耐量的代谢背景:肾上腺素诱导损伤的机制。

Metabolic background for glucose tolerance: mechanism for epinephrine-induced impairment.

作者信息

Skikama H, Ui M

出版信息

Am J Physiol. 1975 Oct;229(4):955-61. doi: 10.1152/ajplegacy.1975.229.4.955.

Abstract

Turnover rates of blood glucose in rats were calculated from the decay of [14C]glucose. A glucose load suppressed glucose appearance and this was reversed by epinephrine or glucagon. Incorporation of [14C]bicarbonate into liver glycogen and blood glucose demonstrated that these hormones did not alter gluconeogetic rate but, rather the proportion of glucose recovered in the two products. The glucose enhanced by glucagon, probably through increased insulin secretion. In contrast, epinephrine decreased peripheral glucose uptake.

摘要

根据[14C]葡萄糖的衰减计算大鼠的血糖周转率。葡萄糖负荷会抑制葡萄糖生成,而肾上腺素或胰高血糖素可使其逆转。[14C]碳酸氢盐掺入肝糖原和血糖的情况表明,这些激素并未改变糖异生速率,而是改变了在这两种产物中回收的葡萄糖比例。胰高血糖素增强葡萄糖生成,可能是通过增加胰岛素分泌实现的。相比之下,肾上腺素会降低外周葡萄糖摄取。

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