严重疟疾感染啮齿动物模型中的低血糖和高胰岛素血症。
Hypoglycemia and hyperinsulinemia in rodent models of severe malaria infection.
作者信息
Elased K, Playfair J H
机构信息
Department of Immunology, University College London Medical School, United Kingdom.
出版信息
Infect Immun. 1994 Nov;62(11):5157-60. doi: 10.1128/iai.62.11.5157-5160.1994.
Abstract
Severe hypoglycemia developed during nonlethal Plasmodium chabaudi and lethal P. yoelii blood stage malaria infection in mice, always in association with hyperinsulinemia. Supernatants of lethal P. yoelii incubated overnight induced hypoglycemia and hyperinsulinemia in normal mice. In murine malaria, hypoglycemia may be largely secondary to increased insulin secretion.
摘要
在小鼠感染非致死性查巴迪疟原虫和致死性约氏疟原虫血期疟疾期间会出现严重低血糖，且总是伴有高胰岛素血症。将致死性约氏疟原虫的培养上清液孵育过夜可诱导正常小鼠出现低血糖和高胰岛素血症。在鼠疟中，低血糖可能很大程度上继发于胰岛素分泌增加。
相似文献
1
Hypoglycemia and hyperinsulinemia in rodent models of severe malaria infection.严重疟疾感染啮齿动物模型中的低血糖和高胰岛素血症。
Infect Immun. 1994 Nov;62(11):5157-60. doi: 10.1128/iai.62.11.5157-5160.1994.
2
Blood-stage malaria infection in diabetic mice.糖尿病小鼠的血液期疟疾感染
Clin Exp Immunol. 1995 Mar;99(3):440-4. doi: 10.1111/j.1365-2249.1995.tb05570.x.
3
Reversal of hypoglycaemia in murine malaria by drugs that inhibit insulin secretion.通过抑制胰岛素分泌的药物逆转小鼠疟疾中的低血糖症。
Parasitology. 1996 Jun;112 ( Pt 6):515-21. doi: 10.1017/s0031182000066087.
4
Early gamma interferon responses in lethal and nonlethal murine blood-stage malaria.致死性和非致死性小鼠血液期疟疾中的早期γ干扰素反应
Infect Immun. 1997 May;65(5):1593-8. doi: 10.1128/iai.65.5.1593-1598.1997.
5
6
Improvement of glucose homeostasis in obese diabetic db/db mice given Plasmodium yoelii glycosylphosphatidylinositols.给予约氏疟原虫糖基磷脂酰肌醇的肥胖糖尿病db/db小鼠的葡萄糖稳态改善。
Metabolism. 2004 Aug;53(8):1048-53. doi: 10.1016/j.metabol.2004.03.013.
7
Correlation of increased expression of intercellular adhesion molecule-1, but not high levels of tumor necrosis factor-alpha, with lethality of Plasmodium yoelii 17XL, a rodent model of cerebral malaria.细胞间黏附分子-1表达增加而非高水平肿瘤坏死因子-α与约氏疟原虫17XL（一种脑型疟疾啮齿动物模型）致死率的相关性。
Am J Trop Med Hyg. 1998 Dec;59(6):852-8. doi: 10.4269/ajtmh.1998.59.852.
8
Transgenic mice expressing human fetal globin are protected from malaria by a novel mechanism.表达人胎儿血红蛋白的转基因小鼠通过一种新机制免受疟疾侵害。
Blood. 1998 Oct 1;92(7):2520-6.
9
Immune responses to defined epitopes of the circumsporozoite protein of the murine malaria parasite, Plasmodium yoelii.针对鼠疟原虫约氏疟原虫环子孢子蛋白特定表位的免疫反应。
Eur J Immunol. 1990 Jun;20(6):1215-22. doi: 10.1002/eji.1830200604.
10
Protective immunity to malaria: studies with cloned lines of rodent malaria in CBA/Ca mice. IV. The specificity of mechanisms resulting in crisis and resolution of the primary acute phase parasitaemia of Plasmodium chabaudi chabaudi and P. yoelii yoelii.疟疾的保护性免疫：CBA/Ca小鼠中啮齿类疟原虫克隆株的研究。IV. 导致查巴迪疟原虫和约氏疟原虫原发性急性期寄生虫血症危机和消退的机制特异性。
Parasite Immunol. 1989 Jan;11(1):1-13. doi: 10.1111/j.1365-3024.1989.tb00644.x.
引用本文的文献
1
Hormones in malaria infection: influence on disease severity, host physiology, and therapeutic opportunities.疟疾感染中的激素：对疾病严重程度、宿主生理和治疗机会的影响。
Biosci Rep. 2024 Nov 27;44(11). doi: 10.1042/BSR20240482.
2
Periodic Parasites and Daily Host Rhythms.寄生虫的周期性与宿主的日常节律。
Cell Host Microbe. 2020 Feb 12;27(2):176-187. doi: 10.1016/j.chom.2020.01.005.
3
The effects of dyslipidaemia and cholesterol modulation on erythrocyte susceptibility to malaria parasite infection.血脂异常和胆固醇调节对红细胞易感性疟疾寄生虫感染的影响。
Malar J. 2019 Nov 29;18(1):381. doi: 10.1186/s12936-019-3016-3.
4
Plasmodium Infection Induces Dyslipidemia and a Hepatic Lipogenic State in the Host through the Inhibition of the AMPK-ACC Pathway.疟原虫感染通过抑制 AMPK-ACC 通路诱导宿主血脂异常和肝脏脂肪生成状态。
Sci Rep. 2019 Oct 11;9(1):14695. doi: 10.1038/s41598-019-51193-x.
5
Adrenal hormones mediate disease tolerance in malaria.肾上腺激素调节疟疾中的疾病耐受。
Nat Commun. 2018 Oct 30;9(1):4525. doi: 10.1038/s41467-018-06986-5.
6
Daily Rhythms of TNFα Expression and Food Intake Regulate Synchrony of Plasmodium Stages with the Host Circadian Cycle.TNFα 表达和摄食的日常节律调节疟原虫阶段与宿主昼夜节律的同步性。
Cell Host Microbe. 2018 Jun 13;23(6):796-808.e6. doi: 10.1016/j.chom.2018.04.016. Epub 2018 May 24.
7
Increased Plasmodium chabaudi malaria mortality in mice with nutritional iron deficiency can be reduced by short-term adjunctive iron supplementation.营养性缺铁导致感染疟原虫的伯氏疟原虫鼠死亡率增加，短期补充铁剂可降低这种死亡率。
Malar J. 2018 Jan 16;17(1):34. doi: 10.1186/s12936-018-2186-8.
8
Pathogen manipulation of host metabolism: A common strategy for immune evasion.病原体对宿主代谢的操控：一种常见的免疫逃避策略。
PLoS Pathog. 2017 Dec 7;13(12):e1006669. doi: 10.1371/journal.ppat.1006669. eCollection 2017 Dec.
9
A Novel Model of Asymptomatic Plasmodium Parasitemia That Recapitulates Elements of the Human Immune Response to Chronic Infection.一种新型无症状疟原虫血症模型，该模型概括了人类对慢性感染的免疫反应要素。
PLoS One. 2016 Sep 1;11(9):e0162132. doi: 10.1371/journal.pone.0162132. eCollection 2016.
10
γδ T cells acquire effector fates in the thymus and differentiate into cytokine-producing effectors in a Listeria model of infection independently of CD28 costimulation.γδ T 细胞在胸腺中获得效应细胞命运，并在李斯特菌感染模型中独立于 CD28 共刺激分化为细胞因子产生效应细胞。
PLoS One. 2013 May 9;8(5):e63178. doi: 10.1371/journal.pone.0063178. Print 2013.
本文引用的文献
1
Immunoassay of insulin with insulin-antibody precipitate.用胰岛素 - 抗体沉淀物进行胰岛素免疫测定。
Biochem J. 1963 Jul;88(1):137-46. doi: 10.1042/bj0880137.
2
Signal transduction in host cells by a glycosylphosphatidylinositol toxin of malaria parasites.疟原虫糖基磷脂酰肌醇毒素在宿主细胞中的信号转导
J Exp Med. 1993 Jan 1;177(1):145-53. doi: 10.1084/jem.177.1.145.
3
Hypoglycaemia and counterregulatory hormone responses in severe falciparum malaria: treatment with Sandostatin.
Q J Med. 1993 Apr;86(4):233-40.
4
Tumor necrosis factor-alpha suppresses insulin-induced tyrosine phosphorylation of insulin receptor and its substrates.肿瘤坏死因子-α抑制胰岛素诱导的胰岛素受体及其底物的酪氨酸磷酸化。
J Biol Chem. 1993 Dec 15;268(35):26055-8.
5
Metabolic disturbances in Plasmodium coatneyi-infected rhesus monkeys.
Int J Parasitol. 1993 Aug;23(5):557-63. doi: 10.1016/0020-7519(93)90160-z.
6
Mechanism of hyperinsulinemia in endotoxicosis.内毒素血症中高胰岛素血症的机制。
Am J Physiol. 1980 Aug;239(2):E156-61. doi: 10.1152/ajpendo.1980.239.2.E156.
7
Severe hypoglycemia and hyperinsulinemia in falciparum malaria.
N Engl J Med. 1983 Jul 14;309(2):61-6. doi: 10.1056/NEJM198307143090201.
8
Quinine and the stimulus-secretion coupling in pancreatic beta-cells: glucose-like effects on potassium permeability and insulin release.奎宁与胰腺β细胞中的刺激-分泌偶联：对钾通透性和胰岛素释放的类葡萄糖效应。
Endocrinology. 1982 Apr;110(4):1325-32. doi: 10.1210/endo-110-4-1325.
9
Effect of islet-activating protein (IAP), purified from the culture medium of Bordetella pertussis, on the secretion of immunoreactive insulin and glucagon in normal, alloxan-treated, and depancreatized dogs.
Diabetes. 1981 May;30(5):430-4. doi: 10.2337/diab.30.5.430.
10
Pathophysiology of Plasmodium berghei infection in mice.伯氏疟原虫感染小鼠的病理生理学
Exp Parasitol. 1965 Dec;17(3):277-86. doi: 10.1016/0014-4894(65)90071-8.
Zotero 插件