Effect of interleukin 1α and interleukin 2 over glucose metabolism in isolated uterus of restricted diet rats. Influence of NO and COX-2

J.A. Linares, M.L. Campos, A. Goldraij
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Abstract

A 25-day dietary restriction (50% of the normal diet) produce a fall in the production of 14CO2 from 14C-glucose in rats isolated uteri. The addition of 10 or 20 ng ml−1 interleukin 1α (IL-1α) or interleukin 2(IL-2) to the Krebs–Ringer bicarbonate solution medium stimulates glucose metabolism in uteri from underfed rats. Such concentrations are not effective in control rats.
The addition of Nω-nitro-l arginine methyl ester—an inhibitor of both the constitutive and inducible forms of nitric oxide synthase (NOS)—and of aminoguadinine—a preferential inhibitor of the inducible form of NOS—block such estimulation.
In other experiments, the addition to the medium of arginine—a substrate for the formation of nitric oxide—increases interleukin stimulation of glucose metabolism, which is blocked by NOS inhibitor. At the same time, NS-398—a selective inhibitor of inducible cyclooxygenase (COX)—eliminates the interleukin metabolism stimulation. We conclude that IL-1α and IL-2 produce an increase of glucose metabolism in uteri isolated from underfed rats. Nitric oxide produced by the inducible form of NOS mediates the interleukins-induced glucose metabolism stimulation with the participation of inducible COX.
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白细胞介素1α和白细胞介素2对限制饮食大鼠离体子宫糖代谢的影响。NO和COX-2的影响
25天的饮食限制(正常饮食的50%)会导致大鼠离体子宫中14c -葡萄糖产生14CO2的下降。在克雷布-林格碳酸氢盐溶液培养基中添加10或20 ng ml -1白细胞介素1α (IL-1α)或白细胞介素2(IL-2)刺激不足喂养大鼠子宫内的葡萄糖代谢。这种浓度对对照大鼠无效。ω-硝基- 1精氨酸甲酯(一氧化氮合酶的组成型和诱导型抑制剂)和氨基胍(一氧化氮合酶的诱导型优先抑制剂)的加入阻断了这种刺激。在其他实验中,在培养基中加入精氨酸(一种形成一氧化氮的底物)会增加白细胞介素对葡萄糖代谢的刺激,而这种刺激被NOS抑制剂阻断。同时,ns -398选择性诱导型环氧合酶(COX)抑制剂可消除白细胞介素代谢刺激。我们的结论是,IL-1α和IL-2在离体喂养不足的大鼠的子宫中引起葡萄糖代谢的增加。诱导型一氧化氮在诱导型COX参与下介导白介素诱导的糖代谢刺激。
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来源期刊
Prostaglandins, leukotrienes, and essential fatty acids
Prostaglandins, leukotrienes, and essential fatty acids Clinical Biochemistry, Endocrinology, Diabetes and Metabolism
CiteScore
5.30
自引率
0.00%
发文量
0
审稿时长
64 days
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