Skip to main content

Home/ Dr. Goodyear/ Group items tagged PPAR-alpha

Rss Feed Group items tagged

Filter: All | Bookmarks | Topics Simple Middle
Nathan Goodyear

Effects of Peroxisome Proliferator-Activated Receptor-α and -γ Agonists on 11... - 0 views

jcem.endojournals.org/...1848.long

11-betaHSD1 PPAR agonist PPAR-alpha PPAR-gamma PPARs cortisol

shared by Nathan Goodyear on 08 Oct 13 - No Cached
  • Nathan Goodyear on 08 Oct 13
     
    PPAR alpha and/or PPAR gamma does not down regulate 11Beta-HSD1.
Nathan Goodyear

Peroxisome proliferator-activated receptors in inflammation control - 0 views

joe.endocrinology-journals.org/...453.short

PPAR PPARs peroxisome proliferator-activated receptors inflammation NF-kapppB PPAR-gamma PPAR-alpha

shared by Nathan Goodyear on 10 Oct 12 - No Cached
  • Nathan Goodyear on 10 Oct 12
     
    PPARs are key regulators in inflammation control. PPARs are nuclear transcription factors that decrease NF-KappaB transcription.
Nathan Goodyear

Peroxisome Proliferator-activated Receptor α Activation Modulates Cellular Re... - 0 views

www.jbc.org/...32833.long

DHEA dehydroepiandrosterone inflammation TNF-alpha NF-KappaB PPAR-alpha

shared by Nathan Goodyear on 30 Jul 13 - No Cached
  • Nathan Goodyear on 30 Jul 13
     
    DHEA inhibits NF-kappaB stimulated TNF-alpha production through regulation of PPAR-alpha.
Nathan Goodyear

Omega-3 Fatty Acids and Inflammatory Processes - 0 views

www.ncbi.nlm.nih.gov/...PMC3257651

fats nutrition diet omega 3 inflammation NF-kappaB TNF-alpha omega-3 fish oil DHA EPA docosahexaenoic acid eicosapentaenoic acid

shared by Nathan Goodyear on 15 Sep 17 - No Cached
  • marine n-3 PUFAs have also been shown to alter the production of inflammatory proteins including chemokines, cytokines, growth factors and matrix proteases
  • Two transcription factors that are likely to play a role in inflammation are nuclear factor κ B (NFκB) and PPAR-γ
  • NFκB is the principal transcription factor involved in upregulation of inflammatory cytokine, adhesion molecule and cyclooxygenase-2 genes
  • ...3 more annotations...
  • PPAR-γ, is believed to act in an anti-inflammatory manner
  • PPAR-γ directly regulates inflammatory gene expression, it also interferes with the activation of NFκB creating an intriguing interaction between these two transcription factors
  • Both NFκB and PPAR-γ may be regulated by n-3 PUFAs.
  • Nathan Goodyear on 15 Sep 17
     
    great review of the anti-inflammatory effects of omega 3 DHA and EPA.  EPA inhibits COX and 5-LOX and their downstream prostaglandin and leukotrienes.  EPA/DHA inhibited endotoxin-stimulated IL-6, IL-8,TNF-alpha, and NFkappaB.
Nathan Goodyear

PLOS ONE: Overexpression of the Mitochondrial T3 Receptor p43 Induces a Shift in Skelet... - 0 views

www.plosone.org/...journal.pone.0002501

mitochondria T3 thyroid hormone hormones muscle PPAR-gamma PPAR PGC1-alpha

shared by Nathan Goodyear on 29 Jun 13 - No Cached
  • Nathan Goodyear on 29 Jun 13
     
    T3 induces beneficial oxidative changes in muscles through its interaction with mitochondrial receptors.  PGC-1alpha and PPAR-gamma were involved in this process.  The important point here is that T3 is increasing oxidative function of muscle through interaction with mitochondria.
Nathan Goodyear

Figure 3 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

www.nature.com/...nrm2391_F3.html

obesity insulin resistance diabetes TNF-alpha PPAR free fatty acids FFA inflammation

shared by Nathan Goodyear on 22 Dec 11 - No Cached
  • Nathan Goodyear on 22 Dec 11
     
    TNF-alpha downregulates PPAR and increases FFA
Nathan Goodyear

Figure 5 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

www.nature.com/...nrm2391_F5.html

obesity insulin resistance diabetes TNF-alpha PPAR free fatty acids FFA inflammation

shared by Nathan Goodyear on 22 Dec 11 - No Cached
  • Nathan Goodyear on 22 Dec 11
     
    proposed TNF-alpha downregulation of PPAR and resultant increase in FFA and thus inflammation, insulin resistance, diabetes...
Nathan Goodyear

Access : Sulforaphane Inhibits Mitotic Clonal Expansion During Adipogenesis Through Cel... - 0 views

www.nature.com/...oby2011388a.html

sulphoraphane obesity overweight weight-loss PPAR-gamma C_EBP-alpha

shared by Nathan Goodyear on 31 Jan 12 - No Cached
  • Nathan Goodyear on 31 Jan 12
     
    sulphoraphane shown to arrest fat cell growth.  Sulphoraphane decreased PPAR-gamma and C/EBP-alpha expression as well as suppressing the cell growth cycle.  Obvious implications in weight loss
Nathan Goodyear

Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content... - 0 views

ajpendo.physiology.org/...E1093

omega-7 n-7 palmitoleic acid PPAR-alpha PPAR

shared by Nathan Goodyear on 14 Nov 13 - No Cached
  • Nathan Goodyear on 14 Nov 13
     
    Palmitoleic acid, an omega-7, is associated with increased lipolysis through PPARalpha.
Nathan Goodyear

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

www.sciencedirect.com/...S0014579307012082

inflammation insulin resistance IR PPAR TNF-alpha IL-6 IL-10 IL-1Beta JNK GLT-4 Resistin adiponectin Gherlin NF-kapppB iNOS lkkb obesity TLR-4

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • 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
  • Nathan Goodyear on 10 Jan 12
     
    Great review of all the known components in the inflammation, insulin resistance link
1 - 10 of 10
Showing 20▼ items per page