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Nathan Goodyear

Toll-like Receptor Status in Obesity and Metabolic Syndrome: A Translational Perspectiv... - 0 views

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    Only the abstract is available publicly.   Toll-like receptors, particularly TLR-4 has been shown to be associated with insulin resistance.  These TLRs have specific pathogen recognition sites.  TLRs are stimulated by fatty acids (FA) and endotoxemia from bacteria.  Thus, dietary intake of high trans fats, inflammation originating from the gut can be the source of insulin receptor dysfunction through TLRs.
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

Involvement of gut microbiota in the developmen... [Gut Microbes. 2012] - PubMed - NCBI - 0 views

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    gut microbiota, and the imbalance of (dysbiosis) contributes to LPS and inflammation.  This results in obesity and type II DM.
Nathan Goodyear

High Glucose-Induced Expression of Proinflammatory Cytokine and Chemokine Genes in Mono... - 0 views

  • HG significantly increased the expression of monocyte chemoattractant protein-1 (MCP-1), TNF-α, β2-integrin, interleukin-1β, and others. HG treatment increased transcription of the MCP-1 gene, MCP-1 protein levels, and adhesion of THP-1 cells to endothelial cells. HG-induced MCP-1 mRNA expression and monocyte adhesion were blocked by specific inhibitors of oxidant stress, protein kinase C, ERK1/2, and p38 mitogen-activated protein kinases
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    High glucose associated with significant increase in inflammatory signaling.
Nathan Goodyear

Diabetologia, Volume 46, Number 5 - SpringerLink - 0 views

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    This study finds obesity associated with inflammation, but insulin resistance not.  But insulin resistance contributes to obesity...
Nathan Goodyear

Gout, diet, and the insulin resistance syndrome. - 1 views

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    Gout is a result of Insulin resistance?  It makes perfect biologic sense.  IR causes inflammation and what is Gout?  Nothing but an inflammatory condition.  So is Gout merely a join representation of metabolic dysfunction?  I say yes.
Nathan Goodyear

Interaction Between Obesity and the Gut Microbiota: Relevance in Nutrition - 0 views

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    Gut inflammation resultant from dysbiosis leads to inflammation, obesity, insulin resistance, type II DM, hypertension...
Nathan Goodyear

Is central obesity, hyperinsulinemia and dyslipidemia associated with high-grade prosta... - 0 views

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    No surprise that insulin resistance, dyslipidemia, and obesity are associated with high-grade prostate cancer.  It's called inflammation.
Nathan Goodyear

Preadipocytes Mediate Lipopolysaccharide-Induced Inflammation and Insulin Resistance in... - 0 views

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    proposed model of how LPS stimulates NF-kappaB activation and the inflammatory cascade.  This plays a key role in the obesity epidemic.
Nathan Goodyear

Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fa... - 0 views

  • high-fat feeding strongly increased intestinal permeability and reduced the expression of genes coding for proteins of the tight junctions
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    changes in the gut flora shown to induce metabolic endotoxemia, inflammation, insulin resistance, and obesity.  Granted, this study was done in mice.
Nathan Goodyear

Effect of a Mediterranean-Style Diet on Endothelial Dysfunction and Markers of Vascular... - 0 views

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    Mediterranean diet shown to reduce hs-CRP, IL-6, IL-7, IL-18, and decreases insulin resistance in those with metabolic syndrome
Nathan Goodyear

Dash diet - 0 views

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    For those interested in learning the DASH diet. The dash diet has been shown to reduce blood pressure, weight, oxidative stress, inflammation, and insulin resistance.
Nathan Goodyear

DASH Diet Lowers Blood Pressure and Lipid-Induced Oxidative Stress in Obesity - 0 views

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    DASH diet shown to lower oxidative stress, inflammation, improve insulin resistance, lower inflammation, and aid weight loss.
Nathan Goodyear

Obesity, adipocytokines, and cancer - 0 views

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    adipocytokines, such as leptin and adiponectin, impact much more than insulin resistance and obesity. Leptin and adiponectin play some role in the development of certain cancers. Bringing together the common thread of inflammation
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
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  • 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

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.
Nathan Goodyear

JCI - Inflammation and insulin resistance - 0 views

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    How does inflammation cause insulin resistance?  This in-depth paper helps to explain the current understanding.  

    More and more obesity is part of a growing inflammatory epidemic.
Nathan Goodyear

Recent advances in the relationship betwee... [Eur Cytokine Netw. 2006] - PubMed - NCBI - 0 views

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    obesity, inflammation and insulin link
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