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1
Lipopolysaccharide-induced insulin resistance in monolayers of cultured hepatocytes.脂多糖诱导培养的肝细胞单层产生胰岛素抵抗。
Br J Exp Pathol. 1989 Apr;70(2):199-205.
2
Effect of Escherichia coli lipopolysaccharide on the microviscosity of liver plasma membranes and hepatocyte suspensions and monolayers.大肠杆菌脂多糖对肝细胞膜、肝细胞悬液和单层细胞微黏度的影响。
Cell Biochem Funct. 1987 Jan;5(1):55-61. doi: 10.1002/cbf.290050107.
3
Normal rat hepatic stellate cells respond to endotoxin in LBP-independent manner to produce inhibitor(s) of DNA synthesis in hepatocytes.正常大鼠肝星状细胞以不依赖脂多糖结合蛋白的方式对内毒素作出反应,从而产生肝细胞DNA合成抑制剂。
J Cell Physiol. 2005 Aug;204(2):654-65. doi: 10.1002/jcp.20366.
4
Escherichia coli lipopolysaccharide effects on proliferating rat liver cells in culture: a morphological and functional study.大肠杆菌脂多糖对培养的大鼠增殖肝细胞的影响:一项形态学和功能研究。
Tissue Cell. 1999 Feb;31(1):1-7. doi: 10.1054/tice.1998.0013.
5
Intracellular calcium alterations and free radical formation evaluated by flow cytometry in endotoxin-treated rat liver Kupffer and endothelial cells.通过流式细胞术评估内毒素处理的大鼠肝脏库普弗细胞和内皮细胞中的细胞内钙变化及自由基形成。
Eur J Cell Biol. 1994 Oct;65(1):200-5.
6
Deacylation of bacterial lipopolysaccharide in rat hepatocytes in vitro.体外大鼠肝细胞中细菌脂多糖的脱酰基作用
Br J Exp Pathol. 1989 Jun;70(3):267-74.
7
Morphological damage induced by Escherichia coli lipopolysaccharide in cultured hepatocytes: localization and binding properties.大肠杆菌脂多糖对培养肝细胞诱导的形态学损伤:定位与结合特性
Br J Exp Pathol. 1988 Aug;69(4):537-49.
8
Inducible nitric oxide synthase plays a role in LPS-induced hyperglycemia and insulin resistance.诱导型一氧化氮合酶在脂多糖诱导的高血糖和胰岛素抵抗中起作用。
Am J Physiol Endocrinol Metab. 2002 Feb;282(2):E386-94. doi: 10.1152/ajpendo.00087.2001.
9
Nitric oxide mediates lipopolysaccharide-induced alteration of mitochondrial function in cultured hepatocytes and isolated perfused liver.一氧化氮介导脂多糖诱导的培养肝细胞和离体灌注肝脏中线粒体功能的改变。
Hepatology. 1993 Aug;18(2):380-8.
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Hepatocyte function in sepsis: Kupffer cells mediate a biphasic protein synthesis response in hepatocytes after exposure to endotoxin or killed Escherichia coli.脓毒症中的肝细胞功能:库普弗细胞在内毒素或灭活大肠杆菌刺激后介导肝细胞的双相蛋白质合成反应。
Surgery. 1985 Sep;98(3):388-95.

引用本文的文献

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Hepatic expression of lipopolysaccharide-binding protein (Lbp) is induced by the gut microbiota through Myd88 and impairs glucose tolerance in mice independent of obesity.脂多糖结合蛋白(Lbp)在肝脏中的表达受肠道菌群通过 Myd88 诱导,且独立于肥胖,会损害小鼠的葡萄糖耐量。
Mol Metab. 2020 Jul;37:100997. doi: 10.1016/j.molmet.2020.100997. Epub 2020 Apr 16.
2
Effect of insulin levels on the phosphorylation of specific amino acid residues in IRS-1: implications for burn-induced insulin resistance.胰岛素水平对胰岛素受体底物-1中特定氨基酸残基磷酸化的影响:对烧伤诱导的胰岛素抵抗的意义。
Int J Mol Med. 2009 Oct;24(4):531-8. doi: 10.3892/ijmm_00000262.
3
Binding studies and localization of Escherichia coli lipopolysaccharide in cultured hepatocytes by an immunocolloidal-gold technique.通过免疫胶体金技术对培养的肝细胞中大肠杆菌脂多糖进行结合研究及定位。
Histochem J. 1991 May;23(5):221-8. doi: 10.1007/BF01462244.

本文引用的文献

1
Fluid endocytosis in isolated rat parenchymal and non-parenchymal liver cells.分离的大鼠肝实质细胞和非实质细胞中的液体胞吞作用。
Exp Cell Res. 1980 Mar;126(1):109-19. doi: 10.1016/0014-4827(80)90475-9.
2
Surface binding and rates of internalization of 125I-insulin in adipocytes and IM-9 lymphocytes.脂肪细胞和IM-9淋巴细胞中125I-胰岛素的表面结合及内化速率
J Biol Chem. 1982 Aug 10;257(15):8667-73.
3
On the mechanism of ligand-induced down-regulation of insulin receptor level in the liver cell.关于配体诱导肝细胞中胰岛素受体水平下调的机制
J Biol Chem. 1981 Feb 25;256(4):1689-94.
4
Insulin hypersecretion and potentiation of endotoxin shock in the rat.大鼠胰岛素分泌过多与内毒素休克的增强作用
Circ Shock. 1982;9(6):589-603.
5
The internalisation of [125I] insulin by isolated rat hepatocytes.
Horm Metab Res. 1982 Oct;14(10):536-9. doi: 10.1055/s-2007-1019070.
6
Dansylcadaverine inhibits internalization of 125I-epidermal growth factor in BALB 3T3 cells.丹磺酰尸胺抑制125I-表皮生长因子在BALB 3T3细胞中的内化。
J Biol Chem. 1980 Feb 25;255(4):1239-41.
7
Effect of Escherichia coli lipopolysaccharide on the glucagon and insulin binding to isolated rat hepatocytes.大肠杆菌脂多糖对胰高血糖素和胰岛素与分离的大鼠肝细胞结合的影响。
Mol Cell Biochem. 1984 Nov;65(1):37-44. doi: 10.1007/BF00226017.
8
Energy metabolism in sepsis: treatment based on different patterns in shock and high output stage.脓毒症中的能量代谢:基于休克期和高排出量期不同模式的治疗
Ann Surg. 1974 May;179(5):684-96. doi: 10.1097/00000658-197405000-00023.
9
Depression of hepatic gluconeogenesis and the hypoglycemia of endotoxin shock.肝糖异生的抑制与内毒素休克的低血糖症
Am J Physiol. 1974 Oct;227(4):778-81. doi: 10.1152/ajplegacy.1974.227.4.778.
10
Impaired gluconeogenesis in dogs with E. coli bacteremia.
Surgery. 1974 Oct;76(4):533-41.

脂多糖诱导培养的肝细胞单层产生胰岛素抵抗。

Lipopolysaccharide-induced insulin resistance in monolayers of cultured hepatocytes.

作者信息

Portolés M T, Pagani R, Ainaga M J, Díaz-Laviada I, Municio A M

机构信息

Department of Biochemistry & Molecular Biology I, Faculty of Chemistry, Universidad Complutense, Madrid, Spain.

出版信息

Br J Exp Pathol. 1989 Apr;70(2):199-205.

PMID:2659062
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2040547/
Abstract

In order to clarify the endotoxin effect on the hepatic removal of insulin, the influence of lipopolysaccharide (LPS) from E. coli 0111:B4 on the insulin binding and endocytosis in cultured hepatocytes from adult male rats has been investigated. LPS decreases both processes in a time and temperature-dependent manner, showing a major effect at short time and low temperature, according to the characteristics of LPS binding and uptake.

摘要

为了阐明内毒素对肝脏清除胰岛素的影响,研究了来自大肠杆菌0111:B4的脂多糖(LPS)对成年雄性大鼠培养肝细胞中胰岛素结合和内吞作用的影响。根据LPS结合和摄取的特性,LPS以时间和温度依赖性方式降低这两个过程,在短时间和低温下显示出主要作用。