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Nathan Goodyear

Vitamin C Inhibits Metastasis of Peritoneal Tumors By Preventing Spheroid Formation in ... - 0 views

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    Vitamin C inhibits M2 macrophages in the TME and inhibits EMT.
Nathan Goodyear

Frontiers | Reprogramming of Tumor-Associated Macrophages with Anticancer Therapies: Ra... - 0 views

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    Chemotherapy and radiation induce M2 macrophage polarization favoring metastasis.
Nathan Goodyear

The interaction of anticancer therapies with tumor-associated macrophages - 0 views

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    Chemotherapy induces TME M2 polarization
Nathan Goodyear

A novel mechanism of lung cancer inhibition by methionine enkephalin through remodeling... - 0 views

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    MENK increased the infiltration of M1-type macrophages, natural killer cells, CD8+ T cells, CD4+ T cells, and dendritic cells into the TME, and decreased the proportion of myeloid inhibitory cells and M2-type macrophages. Plays particular role in preventing immune escape and immune dysfunction paramount to cancer metastasis
Nathan Goodyear

Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 0 views

  • 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
  • Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
  • Insulin is a pleiotropic hormone
  • ...25 more annotations...
  • the percentage of macrophages in a given adipose tissue depot is positively correlated with adiposity and adipocyte size
  • Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes
  • Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NFκB activation by reducing IKK activity [38]
  • adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression
  • One theory holds that the expansion of adipose tissue leads to adipocyte hypertrophy and hyperplasia and that large adipocytes outstrip the local oxygen supply leading to cell autonomous hypoxia with activation of cellular stress pathways
  • The use of the anti-inflammatory compounds, salicylate and its derivative aspirin, for treating symptoms of T2DM dates back over 100 years
  • elevated levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states
  • overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses
  • Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity
  • In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter
  • macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the “classically activated” pro-inflammatory macrophage, to the M2 state or the “alternatively activated” non-inflammatory cell
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes iNOS (reviewed in [33]
  • Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes.
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • elevated JNK activity in liver, adipose tissue and skeletal muscle of obese insulin resistant mice, and knockout of Jnk1 (Jnk1−/−) leads to amelioration of insulin resistance in high fat diet
  • Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance
  • C-reactive protein (CRP)
  • these studies highlight the possibility that increased iNOS activity plays a direct role in the pathogenesis of insulin resistance
  • the important role of Ikkb in the development of obesity and inflammation-induced insulin resistance.
  • It is probable that local concentrations of inflammatory mediators, such as FFAs, Tnf or other cytokines/adipokines contribute to this polarity switch
  • Tnf and other cytokines/chemokines are symptomatic of inflammation, and while they propagate and/or maintain the inflammatory state, they are not the initial cause(s) of inflammation
  • Tlr4, in particular, is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria
  • Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system.
  • Tlr4 stimulation results in the activation of both Ikkb/NFκB and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1, etc. (reviewed in [57
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    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

Curcumin decreases Warburg effect in cancer cells by down-regulating pyruvate... - 0 views

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    Curcumin inhibits PKM2 and thus the Warburg effect in cancer.
Nathan Goodyear

Hypoxia induces macrophage polarization and re-education toward an M2 phenotype in U87 ... - 1 views

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    to be read
Nathan Goodyear

Frontiers | Vitamin C Inhibits Metastasis of Peritoneal Tumors By Preventing Spheroid F... - 0 views

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    Vitamin C inhibits peritoneal metastasis in EOC model
Nathan Goodyear

Adipose Tissue Recruitment of Leukocytes - 0 views

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    good discussion on how adipose tissue recruits macrophages and increases inflammatory signaling initiating insulin resistance.  This reveals how adipose tissue is extremely active.
Nathan Goodyear

ingentaconnect Adipose Tissue Macrophages, Low Grade Inflammation and Insulin Re... - 0 views

  • “M1” or “classically activated” macrophages
  • PPAR-gamma agonists
  • “M2” or an “alternatively activated” anti-inflammatory phenotype
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    ATMs and obesity induced inflammation initiates insulin resistance and thus type II diabetes. The bodies reaction to a fat cell is no different than a bacterial, viral, or parasitic infection.  The body recognizes something (fat) that shouldn't be there and it attempts to destroy it and remove it.
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