Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 0 views
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A subsequent study by Yuan et al. showed that Tnf treatment of 3T3L1 adipocytes induces insulin resistance and that this could be prevented by pretreatment of cells with aspirin
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Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
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Insulin is a pleiotropic hormone
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Reduced activation and increased ina... [J Clin Endocrinol Metab. 2003] - PubMed - NCBI - 0 views
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These observed changes, in correlation with a low T(3)/rT(3) ratio, may represent tissue-specific ways to reduce thyroid hormone bioactivity during cellular hypoxia and contribute to the low T(3) syndrome of severe illness.
Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views
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Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
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intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
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the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
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Antitumor activity of dichloroacetate on C6 glioma cell: in vitro and in vivo evaluation - 0 views
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the oral bioavailability of DCA is nearly 100%
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the oral bioavailability of DCA is almost 100%.
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DCA can penetrate into the traditional chemotherapy sanctuary sites. Interestingly, it was reported that DCA could penetrate across the BBB,30 exhibiting the potential activity for brain therapy.
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Inborn-like errors of metabolism are determinants of breast cancer risk, clinical respo... - 0 views
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We now recognize that human cancers evolve in an environment of metabolic stress. Rapidly proliferating tumor cells deprived of adequate oxygen, nutrients, hormones and growth factors up-regulate pathways that address these deficiencies to overcome hypoxia (HIF), vascular insufficiency (VEGF), growth factor deprivation (EGFR, HER2) and the loss of hormonal support (ER, PR, AR) all to enhance survival and proliferation
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RAS, PI3K, TP53 and MYC
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The results suggest that breast cancer could be preceded by systemic subclinical disturbances in glucose-insulin homeostasis characterized by mild, likely asymptomatic, IEM-like biochemical changes
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Immune responses to malignancies - 0 views
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increased densities of T-cell infiltrates with a high proportion of CD8+ T cells within primary colorectal carcinomas were associated with a significant protection against tumor recurrence
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coexpression of genes mediating cytotoxicity and TH1 adaptive immune responses accurately predicted survival in patients with colorectal carcinoma independently of the metastatic status.
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tumor-specific cytolytic T lymphocytes (CTLs)
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Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer - 0 views
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The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis
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The most important reason for the poor performance of cancer drugs is the remarkable heterogeneity and adaptability of cancer cells. The molecular characteristics of histologically identical cancers are often dissimilar and molecular heterogeneity frequently exists within a single tumour.
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Because GO is far more efficient in generating ATP compared with GLY (producing 36 vs 2 ATP per glucose
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Vitamin C inhibits NO-induced stabilization of HIF-1alpha in HUVECs | Request PDF - 0 views
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