Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The production of interleukin 1 (IL-1) by lipopolysaccharide (LPS)-stimulated myelomonocytic cell lines ML-1, THP-1 and PL-21 was significantly enhanced by the addition of insulin, insulin-like growth factor (IGF)-I or IGF-II into the cell cultures. The IL-1 activity in the supernatants from cell cultures stimulated with LPS and insulin was completely neutralized by anti-IL-1 beta antibody. Anti-IL-1 alpha antibody had no inhibitory effect. Insulin itself did not stimulate IL-1 beta production directly, but increased it in the mitogen activated cells. However, insulin had no enhancing effect on the production of IL-1 alpha by human T cell lymphotropic virus-I (HTLV-I)-infected T cell lines or on IL-2 production by mitogen-stimulated leukemia T cell lines. Thus, insulin and its related cytokines are shown here as other molecules selectively modulating the production of IL-1 beta in myelomonocytic cell lines.
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PMID:Selective enhancement of interleukin 1 beta production in myelomonocytic cell lines by insulin and its related cytokines. 148 10

Release of basic fibroblast growth factor (bFGF) was investigated in bovine retinal endothelial cells (BREC) maintained in monolayer culture. Confluent cells released bFGF into serum-free culture medium or medium containing 5% serum at rates of up to 105.2 and 61.3 pM/day respectively. bFGF release coincided with a decrease in monolayer cell number and increases in lactate dehydrogenase (LDH) concentration and cells and cell-debris particles in the medium, which suggested that cell damage and lysis were responsible for growth-factor release. Maximum bFGF release at 24 h (230 +/- 10 pM) occurred when the cells were treated with lipopolysaccharide (10 micrograms/ml), which also produced the greatest changes in parameters of cell damage. Sub-confluent cells showed little overt damage at 24 h, but released bFGF (78 +/- 20 pM) along with LDH, indicating that some cell lysis had occurred. Insulin-like growth factor 1 (IGF-1) was also released into serum-free culture medium at a rate of 0.34 nM/day, but not into medium containing serum or when the cells were treated with lipopolysaccharide. This implies that the mechanism of IGF-1 release is different from that of bFGF and is not related to cell damage. Culture medium conditioned by BREC stimulated the proliferation of these cells, as measured by an increase in their incorporation of [methyl-3H]thymidine from 7550 +/- 479 to 10467 +/- 924 d.p.m. These results demonstrate that bFGF is released from damaged BREC and that medium conditioned by these cells can stimulate retinal-endothelial-cell proliferation. This strengthens the case for an involvement of this growth factor in retinal neovascularization.
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PMID:Characterization of release of basic fibroblast growth factor from bovine retinal endothelial cells in monolayer cultures. 203 65

The effect of cyclosporin (CsA) on the endotoxin-induced generalized Shwartzman reaction (GSR) was studied in diabetic and nondiabetic rats. After 4.5 wk of diabetes, CsA (20 mg/kg) or intralipid as a control substance was given intraperitoneally daily for 10 days. Next, diabetic rats were given either high-dose (2 mg/kg or low-dose (0.1 mg/kg) endotoxin (Escherichia coli 026:B6 lipopolysaccharide B) as a single injection. The rats were killed at intervals of 1, 4, 8, and 24 h. No significant glomerular thrombi were seen in the nondiabetic control animals, whereas the severity of glomerular thrombi in the diabetic animals was dependent on the presence or absence of CsA, endotoxin dose, and degree of glycemic control. In the diabetic rats, glomerular thrombi occurred maximally at 4 h but were no longer present at 24 h. The CsA/high-dose-endotoxin rats had fewer glomerular thrombi than rats receiving the intralipid/high-dose endotoxin, but this difference was not statistically significant. The CsA/low-dose-endotoxin rats had increased glomerular thrombi compared with the intralipid/low-dose-endotoxin rats (P less than 0.01). Insulin treatment reduced the glomerular capillary thrombi in the CsA/low-dose-endotoxin diabetic animals. Thus, CsA aggravates the GSR with low-dose endotoxin but has no significant effect when high-dose endotoxin is given. Improved glycemic control reduces the GSR in CsA-treated rats. Thus, the interrelationships of diabetes, endotoxin, and CsA on the GSR are complex, and the pathogenesis of these events is unclear.
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PMID:Effect of cyclosporin on generalized Shwartzman reaction in diabetic rats. 221 64

Muscle glutamine concentration ([GLN]) and protein synthesis rate (Ks) have been examined in vivo in well-fed, protein-deficient, starved, and endotoxemic rats. With protein deficiency (8 or 5% casein diet), [GLN] fell from 7.70 to 5.58 and 3.56 mmol/kg in the 8 and 5% diet groups, with Ks falling from 15.42 to 9.1 and 6.84%/day. Three-day starvation reduced [GLN] and Ks to 2.38 mmol/kg and 5.6%/day, respectively. In all these groups food intakes and insulin were generally well maintained (except in the starved group), whereas free 3,5,3'-triiodothyronine (T3) was depressed in the starved and 5% protein group. The E. coli lipopolysaccharide endotoxin (3 mg/kg) reduced [GLN] to 5.85 and 4.72 mmol/kg and Ks to 10.5 and 9.10%/day in two well-fed groups. Insulin levels were increased, and free T3 levels fell. Combined protein deficiency and endotoxemia further reduced [GLN] and Ks to 1.88 mmol/kg and 4.01%/day, respectively, in the 5% protein rats. Changes in both ribosomal activity (KRNA) and concentration (RNA/protein) contributed to the fall in Ks in malnutrition and endotoxemia, although reductions in the RNA concentration were most marked with protein deficiency and reductions in the KRNA dominated the response to the endotoxin. The changes in [GLN] and Ks were highly correlated as were [GLN] and both KRNA and the RNA concentration, and these relationships were unique to glutamine. These relationships could reflect sensitivity of glutamine transport and protein synthesis to the same regulatory influences, and the particular roles of insulin and T3 are discussed, as well as any direct influence of glutamine on protein synthesis.
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PMID:Relationship between glutamine concentration and protein synthesis in rat skeletal muscle. 313 58

The role of hypoglycemia in tumor necrosis factor (TNF) production was examined. TNF was produced from sera of animals presensitized with reticuloendothelial system stimulants after lipopolysaccharide (LPS) challenge. Blood glucose was strongly reduced during TNF production. Glucose administration to presensitized mice (before LPS challenge) caused inhibition of TNF production. Exogenous insulin injection inhibited TNF production in a dose-related manner. Peritoneal exudate cells (PEC) from Propionibacterium acnes-primed mice revealed increased glucose consumption during in vitro TNF production but showed no relationship between the degree of glucose consumption and the ability to produce TNF. Insulin addition to the culture medium caused inhibition of TNF production from PEC, which indicated that insulin may block TNF production from macrophages. Administration of highly purified TNF (without concomitant LPS) induced extensive tumor necrosis but did not induce hypoglycemia; LPS induced moderate necrosis with accompanying hypoglycemia; insulin induced hypoglycemia but did not induce tumor necrosis. It is concluded that hypoglycemia does not accompany the action of TNF.
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PMID:Relationship of hypoglycemia to tumor necrosis factor production and antitumor activity: role of glucose, insulin, and macrophages. 388 59

Activated mouse spleen lymphocytes have increased amounts of the glycolytic enzymes pyruvate kinase and lactate dehydrogenase. No changes were found in hexokinase and in the gluconeogenic enzyme fructose 1,6-diphosphatase. Concanavalin A-activated T cells give higher activities of those enzymes than lipopolysaccharide-activated B lymphoblasts. Insulin treatment results in a stronger increment of the enzyme activity of mitogen-activated cells. Insulin inhibits the initial proliferation induced by either Con A or LPS, but a 50% increase in antibody-forming cells was found in LPS-treated cultures. Insulin may favour the differentiation of activated cells by increasing the rate of the glycolytic pathway.
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PMID:Mitogen-induced changes in glycolytic enzymes of mouse lymphocytes: influence of insulin on cell activation in vitro. 628 69

The principal goal of the present study was to test the hypothesis that cytokines modulate glucose transport in skeletal muscle by increasing nitric oxide production. Cultured L6 skeletal muscle cells were incubated in the presence of tumour necrosis factor-alpha, interferon-gamma or lipopolysaccharide (LPS) alone or in combination for 24 h. Neither cytokines nor LPS alone induced NO production, as measured by nitrite concentrations in the medium. However, when used in combination, the two cytokines significantly stimulated NO production, and this effect was synergistically enhanced by the presence of LPS. Reverse transcriptase-PCR (RT-PCR) analysis revealed that NO release was associated with the induction of inducible (macrophage-type) NO synthase (iNOS). The increase in iNOS expression was confirmed at the protein level by Western-blot analysis and NADPH/diaphorase histochemical staining. Cytokines and LPS markedly increased basal glucose transport in L6 myocytes. Insulin also stimulated basal glucose transport, but significantly less in cells chronically exposed to cytokines/LPS. The sensitivity of L6 muscle cells to insulin-stimulated glucose transport was also significantly decreased by cytokines/LPS treatment. The NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME) inhibited nitrite production in cytokine/LPS-treated cells, and this prevented the increase in basal glucose transport and restored muscle cell responsiveness to insulin. Cytokines/LPS exposure significantly increased GLUT1 transporter protein levels but decreased GLUT4 expression in L6 cells. l-NAME treatment prevented the increase in GLUT1 protein content but failed to restore GLUT4 transporter levels. These results demonstrate that cytokines and LPS affect glucose transport and insulin action by inducing iNOS expression and NO production in skeletal muscle cells. The data further indicate that cytokines and LPS increase the expression of the GLUT1 transporter protein by an NO-dependent mechanism.
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PMID:Cytokines modulate glucose transport in skeletal muscle by inducing the expression of inducible nitric oxide synthase. 923 Jan 32

Induction of nitric oxide synthase by bacterial endotoxin in vivo can be mimicked by treating cultured hepatocytes with a combination of lipopolysaccharide and cytokines (LPS/cytokines), but the role of LPS/cytokine-induced nitric oxide in hepatocyte glucose metabolism is ambiguous. In this study, intermediary metabolite effects on LPS/cytokine-induced hepatocyte nitric oxide synthesis were examined. Pyruvate, lactate, oxaloacetate, and fumarate all showed some inhibitory effects on hepatocyte nitric oxide synthesis. However, these metabolic intermediates could not improve the mitochondrial respiration of LPS/cytokine-treated hepatocytes. Phosphoenolpyruvate carboxykinase activity (or flux) relating factors, glucocorticoids and cAMP, also blocked LPS/cytokine-induced nitric oxide synthesis. Insulin was much less potent than cAMP and glucocorticoids, and phorbol ester did not show any effect on hepatocyte nitric oxide synthesis. These results suggest that LPS/cytokine-induced nitric oxide synthesis is related, at least partly, to phosphoenolpyruvate carboxykinase activity (or flux) in hepatocytes.
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PMID:Role of metabolic intermediates in lipopolysaccharide/cytokine-mediated production of nitric oxide in isolated mouse hepatocytes. 924 Apr 45

In patients with diabetic renal failure, attention must be paid to the prevention of atherosclerosis as well as the preservation of renal function. Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. A low-protein diet (LPD) is recommended for patients with advanced renal disease, but a large proportion of the total caloric intake is supplied from carbohydrates and fat in LPD. Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). Secondly, risk factors of atherosclerosis were measured before and two weeks after the introduction of LPD in patients with diabetic renal failure. LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis.
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PMID:[Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. 939 42

We evaluated the in vitro effect of growth hormone (GH), prolactin (PRL) and insulin treatment of human monocytes on Herpes simplex virus type 1 (HSV-1) infection. GH and PRL increased cell susceptibility to infection which was related to a slight TNF-alpha expression and release. Insulin had no significant effect. Cells activated with lipopolysaccharide (LPS) and then treated with PRL showed a lower susceptibility to HSV infection related to a significant increase in TNF-alpha expression and release. On the contrary, GH and insulin increased the susceptibility to infection of activated cells but did not modify TNF-alpha expression with respect to cells treated only with hormones.
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PMID:TNF-alpha expression and herpes simplex infection in human monocytes treated with growth hormone, prolactin and insulin. 969


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