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发布于:2018-2-10 04:25:13  访问:4 次 回复:0 篇
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Further, the pharmacological profile of BDNF is strikingly similar to that of leptin, an adipocyte-derived satiety hormone that regulates body adiposity and bone mass in part through activation of the sympathetic nervous system. To determine the effect of BDNF on bone mass and metabolism we evaluated BDNF conditional knock out (KO) mice, in which BDNF expression was deleted from the brain through the use of the Cre-loxP recombination system (Rios et al, 2001). In both males and females, at 3 and 6 mo of age, central BDNF deletion leads to a metabolic phenotype characterized by hyperphagia, increased body weight, elevated serum levels of insulin and glucose, and leptin resistance. The mice are hyperactive with upregulation of UCP1 in brown adipose tissue at older ages. The BDNF conditional KO mice also have 40% greater fat pad weight Doxorubicin solubility dmso than wild type littermates, and show evidence of liver steatosis at older ages, thus confirming diabetic status. Regarding the skeletal phenotype, BDNF KO mice have increased femur length (+6%, p<0.01) and greater femoral BMD (+30%, p<0.001) and BMC (+50%, p<0.001). ��CT analysis of the femurs and vertebrae of 3 mo old BDNF KO mice reveal significantly greater trabecular BV/TV (+50% for distal femur, p<0.001 +35% for vertebral body, p<0.001) and mid-femoral LY 294002 cortical thickness (+11 to 17%, p<0.05). Bone microarchitecture was also enhanced at 6 mo of age, with more pronounced effect in females than males. Taken together these data identify a novel non-neurotrophic function for neurotrophins and provide evidence that the BDNF-to-TrkB signaling plays a role in the central regulation of bone homeostasis. Disclosures: Claudia Camerino, None. 1209 PTH Attenuates H2O2- and Glucocorticoid-induced Suppression of Wnt Signaling via an Akt-dependent Mechanism: a Mechanistic www.selleckchem.com Explanation for the Efficacy of Intermittent PTH in Old Age- and Glucocorticoid-induced Osteoporosis.Maria Jose Almeida*, Shoshana Bartell, Stavros Manolagas, Robert Weinstein, Robert Jilka. University of Arkansas for Medical Sciences, USA Intermittent PTH administration is an effective regimen for increasing bone mass and reducing the incidence of fractures in the osteoporosis that occurs with advancing age or with glucocorticoid administration, but the underlying mechanisms are unclear. Studies in mice show that age-related bone loss is due to increased oxidative stress (OS) and a rise in endogenous glucocorticoids, and is associated with reduced Wnt signaling. OS inhibits Wnt signaling by activating FoxOs and diverting ��-catenin from Tcf- to FoxO-mediated transcription, whereas glucocorticoids attenuate Wnt signaling in part by inhibiting Akt phosphorylation leading to activation of GSK3��, a negative regulator of ��-catenin.
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