Nutrition and the regulation of higher animals in hypoxia

高等动物缺氧的营养与调节

• 批准号: 09660143
• 负责人: NAKANO Yoshihisa
• 金额: $ 1.86万
• 依托单位: Osaka Prefecture University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09660143/
• 关键词: Hypoxia; Gastrin; Epo (erythropoietin); GAPDH (glyceraldehydes-3-phosphate dehydrogenase); MBEC4; iNOS; Vitamin BィイD212ィエD2; 低酸素; ビタミンB_<12>欠乏ラット; スレオニンデヒドラターゼ活性; 赤血球分化; 巨赤芽球細胞; VEGF; エリスロポエチン受容体; NO; NO合成酵素; GAPOH; 胃酸分泌制御; アドレナリン; ノルアド

Hyoixia (10.5 or 7.6%OィイD22ィエD2) delayed gastric emptying and suppressed gastric acid secretion in conscious rats. In addition, although the concentration of plasma gastrin, the principal stimulant of gastric acid secretion, increased under hypoxic conditions, the oral administration of HCL abolished the hypoxia-stimulated gastrin release, indicating that the inhibitory effect of hypoxia on gastric acid secretion stimulates gastrin release through positive feedback regulation.The 10.5%OィイD22ィエD2 hypoxia-suppressed gastric acid secretion was restored to nearly the level in normoxia by the adrenal medullectomy. With 7.6%OィイD22ィエD2hypoxia, the operation also caused an increase in the level of gastric acid output, although the extent was lower than that with 10.5%OィイD22ィエD2hypoxia. Similar results were obtained when reserpine, which causes an adrenaergic discharge, was administered. Furthermore, an α2-adrenoceptor blocking agent, yohimbine, almost completely removed the inhibitory effect o … More f 10.5% and 7.6% OィイD22ィエD2hypoxia on gastric and secretion. Epinephrine release is stimulated by 10.5%OィイD22ィエD2hypoxia, and not only epinephrine but also norepinephrine releases are enhanced by 7.6%OィイD22ィエD2hypoxia. It is suggested that the hypoxia-stimulated adrenergic response acts on the α2-adrenoceptor on the vagus cholinergic endings in the gastric wall, and that the deareased acetylcholine release thereby inhibits gastric acid secretion.Epo functioned as a competence factor for RBECs and maximally stimulated DNA synthesis of RBECs at the concentration of 1 U/ml (the serum concentrations of Epo in most animals are in the range 10 - 30 mU/ml under normal physiological conditions and increase more than 100-fold in hypoxemia resulting from anemia and hypoxic exposure). Furthermore, both RBECs and MBECs expressed two form Epo-R mNRA, the authentic form (aEpo-R) and the intron 5-inserted form (15 Epo-R). RBECs had a single class of low affinity (860 pM) binding site for Epo. These results suggest that rat and murine 15Epo-Rs modulate the functions of Epo by competing the binding of Epo with the authentic receptor as a membrane-bound form and a soluble form, respectively, and that Epo acts on endothelial cells as a competent factor when excess Epo is induced by hypoxia.Hypoxia (2%OィイD22ィエD2) stimulated the expression of GAPDH mRNA in all cell typed tested (MBEC4, Hep G2 CHO cells, Ba/F3 cells and rat sooth muscle cells). Some transition metals (CoィイD12+ィエD1, NiィイD12+ィエD1, ZnィイD12+ィエD1 and MnィイD12+ィエD1) and DFX also upregulated the transcription of GAPDH gene in MBEC4, suggesting that GAPDH is regulated through a mechanism, in which heme protein participates. iNOS was also induced in hypoxia and then cGMP was extremely formed, suggesting that cGMP acts as a intracellular information transmitter.Vitamin BィイD212ィエD2 is known as a developmental factor of blood cell. We have studied how the vitamin BィイD212ィエD2 affects on the development of blood cell in hypoxia. Less

Hyoixia（10.5或7.6％OI D22）在意识大鼠中延迟胃排空和抑制胃酸分泌。此外，尽管在缺氧条件下胃酸分泌的主要刺激性血浆胃酸的浓度增加了，但HCL的口服给药消除了低氧刺激的胃酸胃释放，表明缺氧对胃酸的抑制作用对胃酸的抑制作用对胃酸的抑制作用刺激了胃酸抗反馈的速度。胃酸盐均可促进。通过肾上腺脑瘤切除术将几乎恢复到常氧的水平。该手术的胃酸输出水平也增加了，尽管胃酸输出水平也有所增加，尽管该操作的程度低于10.5％OI D22缺氧。当给予抗肾上腺素能排出的储备金时，获得了相似的结果。此外，α2-肾上腺素受体阻断剂Yohimbine几乎完全消除了抑制作用O…更多的F 10.5％和7.6％OI D22缺氧对胃和分泌。肾上腺素的释放受到10.5％OI D22缺氧的刺激，不仅肾上腺素，而且去甲肾上腺素的释放均通过7.6％OI D22缺氧增强。有人提出，缺氧刺激的肾上腺素反应在胃壁上对α2-肾上腺素受体作用于α2-肾上腺素受体，并在胃壁中的胆碱能结束，致命的乙酰胆碱释放，从而抑制胃酸分泌。EPO在RBEC和最大刺激的DNA dna Consessiss rebess andssiss的能力上起作用。在正常生理条件下，大多数动物的EPO在10-30 mU/mL的范围内，由于贫血和低氧暴露引起的低氧血症增加了100倍以上）。此外，RBEC和MBEC均表达了两种形式的EPO-R MNRA，正宗形式（AEPO-R）和内含子5插入形式（15 EPO-R）。 RBEC具有EPO的一类低亲和力（860 pm）结合位点。这些结果表明，大鼠和鼠15EPO-RS通过竞争EPO与真实受体的结合作为膜结合形式和固体形式，通过竞争EPO的结合，而EPO在超过EPO时作用于内皮细胞作为胜任的因子，由epo超过EPO诱导。 （MBEC4，HEP G2 CHO细胞，BA/F3细胞和大鼠舒服肌肉细胞）。某些过渡金属（COII D12+E D1，NII D12+E D1，Zni D12+E D1和MNI D12+E D1）和DFX还更新了MBEC4中GAPDH基因的转录，这表明通过一种机制来调节GAPDH，在该机构中受到质合蛋白的调节，该机制受到质合蛋白的参与。还诱导了缺氧的iNOS，然后极度形成CGMP，表明CGMP充当细胞内信息发射机。维生素BII D212IE D2被称为血细胞的发育因素。我们研究了维生素BII D212IE D2如何影响缺氧血细胞的发展。较少的

项目成果

中野長久: "食を楽しみ健やかに生きるために" 糸川嘉則, 458 (1997)

Nagahisa Nakano：“享受食物，过健康的生活” Yoshinori Itokawa，458 (1997)

Yosihisa Nakano: "The intron 5-inserted form of rat erythropoietin receptor is expressed as a membrane-bound form" Biochimica et Biophysica Acta. 1403. 169-178 (1998)

Yosihisa Nakano：“大鼠促红细胞生成素受体的内含子 5 插入形式以膜结合形式表达”Biochimica et Biophysicala Acta。

Nalano, Y.: "α2-Adrenoceptor-Mediated Antisecretory Effect of Hypoxia in Conscious Rats"Biosci. Biotech. Biochem.. 62(3). 546-549 (1998)

Nalano，Y.：“意识大鼠中缺氧的α2-肾上腺素受体介导的抗分泌作用”Biosci.Biochem.. 546-549 (1998)。

Yoshihisa Nakano: "α2-Adrenoceptor-Mediated Autisecretory Effect of Hypoxia in Conscious Rats" Biosci.Biotech.Biochem.62. 546-549 (1998)

Yoshihisa Nakano：“α2-肾上腺素受体介导的清醒大鼠缺氧的自分泌效应”Biosci.Biotech.Biochem.62 546-549（1998）。

Nakano Yoshihisa: "The intron 5-inserted form of rat erythropoietin receptor is expressed as a membrane-bound form"Biochim.Biophys.Acta. 1403. 169-178 (1998)

Nakano Yoshihisa：“大鼠促红细胞生成素受体的内含子 5 插入形式以膜结合形式表达”Biochim.Biophys.Acta。