Search results for: Leptin Receptor Antibody
#29024103 2017/10/12 Save this To Up
Functional interleukin-6 receptor-α is located to tanycytes at the base of the third ventricle.Interleukin-6 (IL-6) (-) /(-) mice develop mature onset obesity, while intracerebroventricular (ICV) injection of IL-6 decreases obesity in rodents. Moreover, levels of IL-6 in cerebrospinal fluid (CSF) have been reported to be inversely correlated with obesity in humans. Tanycytes lining the base of the 3(rd) ventricle in the hypothalamus have recently been reported to be of importance for metabolism. In the present study, we investigated whether tanycytes could respond to IL-6 in the CSF. With immunohistochemistry using a well characterized antibody directed against the ligand binding receptor for IL-6, IL-6 receptor α (IL-6Rα), it was found that tanycytes, identified by the two markers vimentin and dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32), contained IL-6Rα. There were fewer IL-6Rα on another type of ventricle-lining cells, ependymal cells, identified by the marker glucose transporter-1 (GLUT-1). To ascertain that the immunoreactive IL-6Rα were responsive to IL-6, we injected IL-6 ICV. This treatment increased immunoreactive phosphorylated STAT-3 (pSTAT-3) in tanycytes after 5 min and in cells in the medial part of the arcuate nucleus (ARC) after 5 and 15 min. ICV injection of leptin exerted similar effects. As expected, intraperitoneal (i.p.) injection of leptin also induced pSTAT-3 staining in the hypothalamus, while IP IL-6 injection had little effect on this parameter. ICV or IP injection of vehicle only had no effect on pSTAT3-immunoreactivity. In summary, there are functional IL-6Rα on tanycytes at the bottom of the third ventricle (3V), in line with the possibility that ventricular administration of IL-6 decreases obesity in mice via an effect on this cell type. This article is protected by copyright. All rights reserved.
2480 related Products with: Functional interleukin-6 receptor-α is located to tanycytes at the base of the third ventricle.interleukin 17 receptor C Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rabbit Anti-Leptin recept Rabbit Anti-Nociceptin re Rabbit Anti-VIP receptor Rabbit Anti-Glucocorticoi Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Rabbit Anti-Leptin recept Rabbit Anti-Adiponectin r
#28638873 2017/06/22 Save this To Up
PROTECTIVE EFFECT OF CAMEL MILK AS ANTI-DIABETIC SUPPLEMENT: BIOCHEMICAL, MOLECULAR AND IMMUNOHISTOCHEMICAL STUDY.Diabetes is a serious disease affects human health. Diabetes in advanced stages is accompanied by general weakness and alteration in fats and carbohydrates metabolism. Recently there are some scientific trends about the usage of camel milk (CM) in the treatment of diabetes and its associated alterations. CM contains vital active particles with insulin like action that cure diabetes and its complications but how these effects occur, still unclear.
1392 related Products with: PROTECTIVE EFFECT OF CAMEL MILK AS ANTI-DIABETIC SUPPLEMENT: BIOCHEMICAL, MOLECULAR AND IMMUNOHISTOCHEMICAL STUDY.anti CD16 monoclonal anti Mouse anti-chick type I c Mouse anti-chick type I c Mouse anti-bovine type I Mouse anti-bovine type I Mouse anti-porcine type I Mouse anti-porcine type I Mouse anti-human type I c Mouse anti-mouse type I c Mouse anti-mouse type I c Rat anti-chick type I col Rat anti-chick type I col
#28542577 2017/05/25 Save this To Up
Leptin signals via TGFB1 to promote metastatic potential and stemness in breast cancer.Epidemiological studies have shown obesity to be linked with poorer outcomes in breast cancer patients. The molecular mechanisms responsible for the increased risk of invasive/metastatic disease with obesity are complex, but may include elevated levels of adipokines such as leptin. Using physiological levels of leptin found in obesity in a novel chronic in vitro treatment model (≤200 ng/ml for 14 days), we confirmed the occurrence of leptin-mediated changes in growth, apoptosis and metastatic behavior, and gene expression changes representing epithelial-to-mesenchymal transition (EMT) and a cancer stem cell (CSC) like phenotype in breast epithelial and cancer cell lines (MCF10A, MCF10AT1, MCF7 and MDA-MB-231). Further, we have discovered that these effects were accompanied by increased expression of TGFB1, and could be significantly reduced by co-treatment with neutralizing antibody against TGFB1, indicating that the induction of these characteristics was mediated via TGFB1. Occurring in both MCF7 and MCF10AT1 cells, it suggests these actions of leptin to be independent of estrogen receptor status. By linking leptin signalling to the established TGFB1 pathway of metastasis / EMT, this study gives a direct mechanism by which leptin can contribute to the poorer outcomes of obese cancer patients. Inhibitors of TGFB1 are in currently in phase III clinical trials in other malignancies, thus identifying the connection between leptin and TGFB1 will open new therapeutic opportunities for improving outcomes for obese breast cancer patients.
1467 related Products with: Leptin signals via TGFB1 to promote metastatic potential and stemness in breast cancer.Breast cancer and matched Breast cancer and matched Breast cancer and matched Top 4 types of cancer (co Top 4 types of cancer (co Top five cancer tissue ar Breast cancer tissue arra Breast cancer (IDC) tissu Breast cancer and adjacen Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra
#28521869 2017/05/19 Save this To Up
High FGF21 levels are associated with altered bone homeostasis in HIV-1-infected patients.Fibroblast growth factor-21 (FGF21) has emerged as an important regulator of glucose, lipid, and body weight homeostasis. However, recent experimental studies have reported that increased FGF21 levels may lead to bone loss.
1192 related Products with: High FGF21 levels are associated with altered bone homeostasis in HIV-1-infected patients.HIV 1 intergase antigen. anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Goat Anti-Human, Mouse AR HIV Self Test Kit, 1Test HIV I&II test strip, Infe Recombinant HIV-1 pol Int Recombinant HIV-1 pol Int Recombinant HIV-1 pol Int Recombinant HIV-1 p31 Int Recombinant HIV-1 p31 Int
#28487437 2017/05/10 Save this To Up
Hypoglycemic Effect of Combined Ghrelin and Glucagon Receptor Blockade.Glucagon receptor (GcgR) blockade has been proposed as an alternative to insulin monotherapy for treating type 1 diabetes since deletion or inhibition of GcgRs corrects hyperglycemia in models of diabetes. The factors regulating glycemia in a setting devoid of insulin and glucagon function remain unclear but may include the hormone ghrelin. Not only is ghrelin release controlled by glucose but also ghrelin has many actions that can raise or reduce falls in blood glucose level. Here, we tested the hypothesis that ghrelin rises to prevent hypoglycemia in the absence of glucagon function. Both GcgR knockout (Gcgr(-/-)) mice and db/db mice that were administered GcgR monoclonal antibody displayed lower blood glucose levels accompanied by elevated plasma ghrelin levels. Although treatment with the pancreatic β-cell toxin streptozotocin induced hyperglycemia and raised plasma ghrelin levels in wild-type mice, hyperglycemia was averted in similarly treated Gcgr(-/-) mice and the plasma ghrelin level was further increased. Notably, administration of a ghrelin receptor antagonist further reduced blood glucose levels into the markedly hypoglycemic range in overnight-fasted, streptozotocin-treated Gcgr(-/-) mice. A lowered blood glucose level also was observed in overnight-fasted, streptozotocin-treated ghrelin receptor-null mice that were administered GcgR monoclonal antibody. These data suggest that when glucagon activity is blocked in the setting of type 1 diabetes, the plasma ghrelin level rises, preventing hypoglycemia.
Glucagon receptor Glucagon like peptide 1 r Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Screen Quest™ Glucagon- AZD-3514 Mechanisms: Andr Rabbit Anti-Human Androge Goat Anti-Human Androgen CAR,Car,Constitutive andr
#28469599 2017/05/04 Save this To Up
The Role of Thyrotropin Receptor Activation in Adipogenesis and Modulation of Fat Phenotype.Evidence from clinical and experimental data suggests that thyrotropin receptor (TSHR) signaling is involved in energy expenditure through its impact on white adipose tissue (WAT) and brown adipose tissue (BAT). TSHR expression increases during mesenchymal stem cell (MSC) differentiation into fat. We hypothesize that TSHR activation [TSHR*, elevated thyroid-stimulating hormone, thyroid-stimulating antibodies (TSAB), or activating mutation] influences MSC differentiation, which contributes to body composition changes seen in hypothyroidism or Graves' disease (GD). The role of TSHR activation on adipogenesis was first investigated using ex vivo samples. Neck fat (all euthyroid at surgery) was obtained from GD (n = 11, TSAB positive), toxic multinodular goiter (TMNG, TSAB negative) (n = 6), and control patients with benign euthyroid disease (n = 11, TSAB negative). The effect of TSHR activation was then analyzed using human primary abdominal subcutaneous preadipocytes (n = 16). Cells were cultured in complete medium (CM) or adipogenic medium [ADM, containing thiazolidinedione (TZD), PPARγ agonist, which is able to induce BAT formation] with or without TSHR activation (gain-of-function mutant) for 3 weeks. Adipogenesis was evaluated using oil red O (ORO), counting adipogenic foci, qPCR measurement of terminal differentiation marker (LPL). BAT [PGC-1α, uncoupling protein 1 (UCP1), and ZIC1], pre-BAT (PRDM16), BRITE- (CITED1), or WAT (LEPTIN) markers were analyzed by semiquantitative PCR or qPCR. In ex vivo analysis, there were no differences in the expression of UCP1, PGC-1α, and ZIC1. BRITE marker CITED1 levels were highest in GD followed by TMNG and control (p for trend = 0.009). This was associated with higher WAT marker LEPTIN level in GD than the other two groups (p < 0.001). In primary cell culture, TSHR activation substantially enhanced adipogenesis with 1.4 ± 0.07 (ORO), 8.6 ± 1.8 (foci), and 5.5 ± 1.6 (LPL) fold increases compared with controls. Surprisingly, TSHR activation in CM also significantly increased pre-BAT marker PRDM16; furthermore, TZD-ADM induced adipogenesis showed substantially increased BAT markers, PGC-1α and UCP1. Our study revealed that TSHR activation plays an important role in the adipogenesis process and BRITE/pre-BAT formation, which leads to WAT or BAT phenotype. It may contribute to weight loss as heat during hyperthyroidism and later transforms into WAT posttreatment of GD when patients gain excess weight.
1058 related Products with: The Role of Thyrotropin Receptor Activation in Adipogenesis and Modulation of Fat Phenotype.Androgen Receptor (Phosph Androgen Receptor (Phosph Interferon-a Receptor Typ Mouse Anti-Human Interleu Rabbit Anti-Human Androge Rabbit Anti-Human Androge Stat3 Activation Inhibito EtBr Destaining Bag Kit A Androgen Receptor (Ab 650 interleukin 17 receptor C interferon-alpha receptor Leptin ELISA Kit, Rat Lep
#28450417 2017/04/28 Save this To Up
GDF11 Attenuates Development of Type 2 Diabetes via Improvement of Islet β-Cell Function and Survival.Growth differentiation factor 11 (GDF11) has been implicated in the regulation of islet development and a variety of aging conditions, but little is known about the physiological functions of GDF11 in adult pancreatic islets. Here, we showed that systematic replenishment of GDF11 not only preserved insulin secretion but also improved the survival and morphology of β-cells and improved glucose metabolism in both nongenetic and genetic mouse models of type 2 diabetes (T2D). Conversely, anti-GDF11 monoclonal antibody treatment caused β-cell failure and lethal T2D. In vitro treatment of isolated murine islets and MIN6 cells with recombinant GDF11 attenuated glucotoxicity-induced β-cell dysfunction and apoptosis. Mechanistically, the GDF11-mediated protective effects could be attributed to the activation of transforming growth factor-β/Smad2 and phosphatidylinositol-4,5-bisphosphate 3-kinase-AKT-FoxO1 signaling. These findings suggest that GDF11 repletion may improve β-cell function and mass and thus may lead to a new therapeutic approach for T2D.
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#28435397 2017/04/24 Save this To Up
Leptin receptor Q223R polymorphism in Egyptian female patients with breast cancer.Breast cancer is the most common cause of death in women. Obesity has been associated with increased risk of breast cancer in post-menopausal women. It induces chronic inflammation, which increases local and systemic levels of cytokines and adipokines such as leptin. Leptin (LEP) and leptin receptor (LEPR) genes have several polymorphisms in humans. This study aims to assess the association between blood levels of leptin and LEPR Q223R gene polymorphism in patients of cancer breast.
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#28174792 2017/02/08 Save this To Up
Antifibrotic action of telmisartan in experimental carbon tetrachloride-induced liver fibrosis in Wistar rats.Liver fibrosis is the increasingly accumulation of extracellular matrix (ECM), caused by chronic liver injuries, and represents a difficult clinical challenge in the entire world. Currently, the advanced knowledge of the cellular and molecular mechanisms of liver fibrosis showed that collagen-producing cells, like activated hepatic stellate cells (HSCs), portal fibroblasts and myofibroblasts are activated by fibrogenic cytokines, such as angiotensin II, transforming growth factor-beta 1 (TGF-β1), and leptin. Because of these, we tested telmisartan, an angiotensin II (AT1) receptor blocker and a peroxisome proliferator-activated receptor-γ (PPARγ) partial agonist, for investigate its antifibrotic action, on experimental model of carbon tetrachloride-induced liver fibrosis.
1937 related Products with: Antifibrotic action of telmisartan in experimental carbon tetrachloride-induced liver fibrosis in Wistar rats.Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Mouse Epstein-Barr Virus TGF beta induced factor 2 Alkaline Phospatase (ALP)
#28122051 2017/01/25 Save this To Up
Low Cytochrome Oxidase 1 Links Mitochondrial Dysfunction to Atherosclerosis in Mice and Pigs.Cytochrome oxidase IV complex regulates energy production in mitochondria. Therefore, we determined the relation of COX genes with atherosclerosis in mice and pigs.
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