Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipodystrophy (LD) with varying degrees of lipohypertrophy, lipoatrophy, hyperlipidemia, and insulin resistance is one of the complications of highly active antiretroviral therapy (HAART) and occurs in one to 33 % of HAART-treated, HIV infected children. We summarize the data on the role of leptin, adiponectin, the growth hormone axis, glucocorticoids, sterol response element binding protein 1c (SREBP-1c), the tumor necrosis factor alpha axis (TNF-alpha), interleukin-6 (IL-6), interleukin- 18 (IL-18), interferon-alpha (IFN-alpha), tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI-1) in the pathophysiology of LD. Adiponectin levels are generally decreased in LD, whereas leptin levels are increased. Systemic cortisol levels are not elevated in LD, even though glucocorticoids seem to play an important role in LD and the phenotype can be reminiscent of Cushing syndrome. GH resistance in LD needs to be better characterized. While some cytokines show promise as markers for LD, it is difficult to tell whether their derangement is a cause of or the effect of LD.
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PMID:HIV--associated lipodystrophy in children. 1636 13

Crohn's disease and ulcerative colitis are inflammatory diseases of the gastrointestinal tract characterized by chronic relapsing inflammation and catabolism. Growth hormone/insulin-like growth factor-I axis is important in inflammatory bowel disease, because of the effects on epithelial cell kinetics, collagen deposition and immunomodulation. The potential of growth hormone as a therapeutic option in inflammatory bowel disease has been proven in various clinical settings. Acquired growth hormone resistance in inflammatory bowel disease seems to be mediated by a combination of undernutrition and active inflammation. In particular, proinflammatory cytokines, such as TNF-a and interleukin-6, have been implicated as potential mediators of growth hormone resistance. The introduction of anti-TNF-alpha monoclonal antibodies has proven very efficacious in patients with inflammatory bowel disease. By reducing cytokines levels in inflammatory cells of intestinal mucosa, infliximab could interfere with cytokine-induced growth hormone resistance. Recent in vivo data have shown that acquired growth hormone resistance in patients with inflammatory bowel disease may be reversed after the administration of anti-TNF-alpha therapy.
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PMID:Growth hormone in inflammatory bowel disease. 1649 5

In this retrospective and quantitated study on banked tissue we found that, compared to normal uterine epithelial cells, growth hormone (GH) is increased 3.4-fold in endometriosis and 3.8-fold in endometrial adenocarcinoma. Similarly, interleukin-6 (IL-6) is increased 2.4-fold in endometriosis and 4.4-fold in endometrial adenocarcinoma. These proteins appear to be involved in the progression of both these conditions. GH is particularly interesting in this context since it is known to not only promote cellular proliferation but also reduces cell-cell adhesion, thus allowing individual cells to break away from their parent architecture. Our results suggest that both IL-6 and GH may play a role in the progression of both endometriosis and endometrial carcinoma.
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PMID:Human growth hormone and interleukin-6 are upregulated in endometriosis and endometrioid adenocarcinoma. 1656 64

Exercise-induced growth hormone (GH) secretion may significantly modulate growth and development in children. Altered physiological GH responses, therefore, may reduce the beneficial effects of exercise. High-fat food ingestion before exercise blunts the GH response in adults, but it is unknown whether this occurs in children. We therefore performed standard exercise tests, following a high-fat meal or placebo, in 12 children, age 11-15 (6 M, 6 F). GH, insulin-like growth factor-I, glucose, insulin, glucagon, cortisol, epinephrine and interleukin-6 samples were drawn at baseline, end-exercise, and 30 and 60 min post-exercise. While GH was similar at baseline in all experiments, the exercise-induced GH peak was lower after the high-fat meal (6.7 +/- 1.6 ng/l vs 11.8 +/- 2.4 ng/l, p <0.02). Other exercise responses were not affected by prior fat ingestion. A high-fat meal before exercise, therefore (a common event in Western societies), may reduce the growth factor response to exercise in children, with potential implications for growth and development.
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PMID:Effect of a high-fat meal on the growth hormone response to exercise in children. 1688 85

Three experiments were conducted to investigate the effects of beta-glucan supplementation on pig performance and immune function. In Exp. 1, 100 weaned pigs (8.65 +/- 0.42 kg of BW and 28 +/- 2 d of age) were used in a 35-d experiment to determine the effects of graded levels of beta-glucan. Pigs were randomly allotted to 1 of 5 treatments containing beta-glucan supplemented at 0, 25, 50, 100, or 200 ppm. Each treatment was replicated using 5 pens containing 4 pigs per pen. The ADG of pigs between d 14 to 28 and d 0 to 28 responded to dietary beta-glucan in a quadratic fashion (P < 0.05), whereas beta-glucan had no effect on ADFI and G:F in any period. In Exp. 2, 80 crossbred pigs (8.23 +/- 0.56 kg of BW and 28 +/- 2 d of age) were used in a 35-d experiment. Pigs were allotted to 1 of 2 dietary treatments (0 or 50 ppm of beta-glucan in the diet) using 10 pens with 4 pigs per pen. Pigs treated with beta-glucan had greater ADG in the 14- to 28-d (P = 0.05) and 0-to 28-d (P = 0.035) periods. The ADFI of pigs receiving beta-glucan was increased (P < 0.05) in the periods from 0 to 14, 0 to 28, and 28 to 35 d. The lymphocyte proliferation index in response to phytohemagglutinin (P = 0.051) and concanavalin A (P = 0.052) tended to decrease on d 14 in pigs supplemented with beta-glucan compared with pigs without supplementation. In Exp. 3, 24 barrows (8.89 +/- 0.20 kg of BW and 28 d of age) were used to investigate the immunological and somatotropic responses of pigs challenged with lipopolysaccharide (LPS). Experimental treatments were arranged in a 2 x 2 factorial, with the main effects of LPS challenge (saline vs. LPS) and dietary addition of beta-glucan (0 vs. 50 ppm). Pigs were raised individually in metabolic cages. Pigs were fed 0 or 50 ppm of beta-glucan for 28 d and then challenged with LPS (25 microg/kg of BW) or saline. After LPS injection, blood was obtained at 0, 1.5, 3, 4.5, 6, and 7.5 h to determine cytokine production and the somatotropic response. Dietary beta-glucan increased plasma interleukin-6 at 1.5, 3, and 4.5 h and tumor necrosis factor-alpha at 3 and 4.5 h and increased plasma interleukin-10 from 3 to 7.5 h after LPS challenge. The beta-glucan treatments had no effect on growth hormone. In conclusion, beta-glucan can selectively influence performance and partially offer benefits on somatotropic axis and immune function in weaned piglets challenged with LPS.
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PMID:Effects of beta-glucan extracted from Saccharomyces cerevisiae on growth performance, and immunological and somatotropic responses of pigs challenged with Escherichia coli lipopolysaccharide. 1690 40

Increased mortality due to cardiovascular disease has been described in adult patients with untreated growth hormone (GH) deficiency. GH replacement therapy has been demonstrate to improve vascular reactivity and reverses early atherosclerotic changes in GH deficient adults. The objective of this study was the assessment of fibrinolytic markers, soluble adhesion molecules, inflammatory cytokines and endothelial function in hypopituitary adults with GH deficiency and with GH replacement therapy. We studied 20 GH deficient patients, 10 men and 10 women (aged, 43.4 +/- 8.4 years) under GH replacement therapy compared with a control group matched for age and body mass index, 9 men and 16 women. All subjects, patients and controls, were life-long non-smokers, normotensive and non-diabetic. The following variables were recorded: anthropometrical and body composition variables, serum concentrations of glucose, insulin and C-peptide; thrombin anti-thrombin fragments and fibrin degradation product D-dimer that were determined by an enzyme-linked-immunosorbent assay (ELISA); IGF-I by radioimmunoassay; C-reactive protein by highly sensitive immunonephelometry; E-selectine, P-selectine, soluble intercellular cell adhesion molecule-1, soluble vascular cell adhesion molecule-1, interleukin-6 and monocyte chemoattractant protein-1 by ELISA. The assessment of endothelial function in vivo was measured by Doppler. Patients with GH deficiency had higher hip/waist ratio and C-peptide and triglycerides concentrations than controls. Our results demonstrated no difference in fibrinolytic markers among patients and controls. E-selectin concentrations were higher in patients than in controls, 22.5+/-11.4 vs. 10.7+/-6.2 microg/L, p = 0.0001. P-selectin, soluble intercellular cell adhesion molecule-1, soluble vascular cell adhesion molecule-1, interleukin-6, monocyte chemoattractant protein-1 and C-reactive protein were similar in the 2 groups. Vascular reactivity and carotid intima-media thickness were also similar in patients and controls. In this study we have demonstrated in adults with GH deficiency under GH substitution elevation of E-selectin concentrations that may correlate with potential endothelial dysfunction suggesting that the protective effect of GH in these patients may be enhancing other mechanisms.
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PMID:Elevation of E-selectin concentrations may correlate with potential endothelial dysfunction in individuals with hypopituitarism during therapy with growth hormone. 1731 45

Gram-negative sepsis with release of endotoxin is a frequent cause of cachexia that develops partly because of resistance to growth hormone (GH) with reduced insulin-like growth factor-I (IGF-I) expression. We set out to more fully characterize the mechanisms for the resistance and to determine whether in addition to a defect in the janus kinase 2 (JAK2)-signal transducer and activator of transcription (STAT) 5b pathway, required for GH-induced IGF-I expression, there might also be a more distal defect. Conscious rats were given endotoxin and studied 4 h later. In liver of these animals, GH-induced JAK2 and STAT5 phosphorylation was impaired and appeared to be caused, at least in part, by a marked increase in hepatic tumor necrosis factor-alpha and interleukin-6 mRNA expression accompanied by elevated levels of inhibitors of GH signaling, namely cytokine-inducible suppressors of cytokine signaling-1 and -3 and cytokine-inducible SH2 protein (CIS). Nuclear phosphorylated STAT5b levels were significantly depressed to 61% of the control values and represent a potential cause of the reduced GH-induced IGF-I expression. In addition, binding of phosphorylated STAT5b to DNA was reduced to an even greater extent and averaged 17% of the normal control value. This provides a further explanation for the impaired IGF-I gene transcription. Interestingly, when endotoxin-treated rats were treated with GH, there was a marked increase in proinflammatory cytokine gene expression in the liver. If such a response were to occur in humans, this might provide a partial explanation for the adverse effect of GH treatment reported in critically ill patients.
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PMID:Endotoxin attenuates growth hormone-induced hepatic insulin-like growth factor I expression by inhibiting JAK2/STAT5 signal transduction and STAT5b DNA binding. 1732 69

Pioglitazone is widely used for the treatment of diabetic patients with insulin resistance. The mechanism of pioglitazone to improve insulin sensitivity is not fully understood. Recent studies have shown that the induction of suppressor of cytokine signaling 3 (SOCS3) is related to the development of insulin resistance. Here, we examined whether the insulin-sensitizing effect of pioglitazone affects the SOCS induction. In db/db mice and high-fat-fed mice, expression of SOCS3 mRNA in fat tissue was increased compared with that in lean control mice, and pioglitazone suppressed SOCS3 levels. In 3T3-L1 adipocytes, mediators of insulin resistance such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6, growth hormone, and insulin increased SOCS3 expression, which was partially inhibited by pioglitazone. The ability of pioglitazone to suppress SOCS3 induction by TNF-alpha was greatly augmented by peroxisome proliferator-activated receptor gamma overexpression. SOCS3 overexpression and tyrphostin AG490, a Janus kinase 2 inhibitor, or dominant-negative STAT3 expression partially inhibited adiponectin secretion and was accompanied by decreased STAT3 phosphorylation. Conversely, pioglitazone increased adiponectin secretion and STAT3 phosphorylation in fat tissue of db/db mice and in 3T3-L1 adipocytes. These results suggest that pioglitazone exerts its effect to improve whole-body insulin sensitivity in part through the suppression of SOCS3, which is associated with the increase in STAT3 phosphorylation and adiponectin production in fat tissue.
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PMID:Effects of pioglitazone on suppressor of cytokine signaling 3 expression: potential mechanisms for its effects on insulin sensitivity and adiponectin expression. 1732 50

Tuberculosis (TB) may be regarded as a disease in which the immune response to Mycobacterium tuberculosis, its etiologic agent, is engaged both in protection and pathology. Different T-lymphocyte subsets are involved in the immune response against M. tuberculosis, but production of interferon-gamma (IFN-gamma) by T cells seems to be fundamental for disease control. Th1-type cytokine responses predominate in patients with mild or moderate forms of pulmonary TB, whereas the production of Th2-type cytokines prevails in the severe disease. Since the immune response fails to definitely eradicate the pathogen, a chronic infection is established, and it is likely that a broad range of regulatory mechanisms operate in this situation. Cytokines released during the course of an immune response activate the hypothalamus-pituitary-adrenal axis leading to the production of glucocorticoids and dehydroepiandrosterone (DHEA), with known immunomodulatory effects. TB patients exhibit increased concentrations of interleukin-6 and cortisol in plasma, reduced DHEA and testosterone levels, together with remarkably increased growth hormone concentrations that were not accompanied by an expected raise in insulin-like growth factor-1. Significant increases in estradiol, prolactin, and thyroid hormone concentrations were also detected in patients. Cortisol inhibits the mycobacterial antigen-driven proliferation and IFN-gamma production, whereas DHEA suppresses transforming growth factor beta production by lymphoid cells from TB patients with advanced disease. Furthermore, supernatants from cultures of M. tuberculosis-stimulated mononuclear cells of TB patients inhibit DHEA secretion by a human adrenal cell line. This type of immuno-endocrine interactions may affect the control of tissue damage and the development of protective immune responses, partly accounting for disease aggravation.
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PMID:The immuno-endocrine component in the pathogenesis of tuberculosis. 1763 94

This study examined the effect of 20 weeks resistance training on a range of serum hormones and inflammatory markers at rest, and following acute bouts of exercise in prostate cancer patients undergoing androgen deprivation. Ten patients exercised twice weekly at high intensity for several upper and lower-body muscle groups. Neither testosterone nor prostate-specific antigen changed at rest or following an acute bout of exercise. However, serum growth hormone (GH), dehydroepiandrosterone (DHEA), interleukin-6, tumor necrosis factor-alpha and differential blood leukocyte counts increased (P < 0.05) following acute exercise. Resistance exercise does not appear to compromise testosterone suppression, and acute elevations in serum GH and DHEA may partly underlie improvements observed in physical function.
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PMID:Endocrine and immune responses to resistance training in prostate cancer patients. 1763 62


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