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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
Nathan Goodyear

Influence of tumor necrosis factor α inhibitors on testicular function and se... - 0 views

www.fertstert.org/...abstract

TNF-alpha sperm motility low T Testosterone LH FSH autoimmune disease inflammation male men hormone hormones

shared by Nathan Goodyear on 18 Feb 14 - No Cached
  • Nathan Goodyear on 18 Feb 14
     
    Cause and effect cannot be taken from this study.  However, TNF-alpha is known to disrupt testicular function, in this case the study found decreased sperm motility, lower Testosterone levels, and increased LH and FSH at baseline.  Improvement was seen after anti-TNF-alpha therapy. The point of this study should be why the elevated TNF-alpha and attack there.
Nathan Goodyear

Diet-induced obesity and low testosterone increase neuroinflammation and impair neural ... - 0 views

www.ncbi.nlm.nih.gov/...PMC4190446

Testosterone neuroinflammation glia insulin resistance obesity diabetes brain CNS PNS inflammation low T low Testosterone TNF-alpha IL-1beta

shared by Nathan Goodyear on 28 Apr 15 - No Cached
  • both obesity and low testosterone are also risk factors for neural dysfunction, including cognitive impairment [58–61] and development of AD
  • Levels of obesity and testosterone are often inversely correlated
  • diet-induced obesity causes significant metabolic disturbances and impairs central and peripheral nervous systems.
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  • both obesity and low testosterone are linked with promotion of inflammatory pathways [70–72] and exert harmful actions on the central [73–75] and peripheral [29,76] nervous systems
  • In general, obesity-related changes were worsened by low testosterone and improved by testosterone treatment; however, this relationship was not statistically significant in several instances. Further, our data suggest that a common pathway that may contribute to obesity and testosterone effects is regulation of inflammation
  • fasting blood glucose levels were independently and additively increased by GDX-induced testosterone depletion and high-fat diet
  • testosterone treatment significantly reduced fasting glucose under both the normal and high-fat diets, demonstrating potential therapeutic efficacy of testosterone supplementation
  • fasting insulin, insulin resistance (HOMA index), and glucose tolerance, low testosterone tended to exacerbate and or testosterone treatment improved outcomes.
  • testosterone status did not significantly affect body weight
  • testosterone’s effects likely do not indicate an indirect result on adiposity but rather regulatory action(s) on other aspects of metabolic homeostasis
  • Prior work in rodents has shown diet-induced obesity induces insulin resistance in rat brain [63] and that testosterone replacement improves insulin sensitivity in obese rats [64]. Our findings are consistent with the human literature, which indicates that (i) testosterone levels are inversely correlated to insulin resistance and T2D in healthy [30,65] as well as obese men [66], and (ii) androgen therapy can improve some metabolic measures in overweight men with low testosterone
  • it has been shown that TNFα has inhibitory effects on neuron survival, differentiation, and neurite outgrowth
  • Our data demonstrate that low testosterone and obesity independently increased cerebrocortical mRNA levels of both TNFα and IL-1β
  • Testosterone status also affected metabolic and neural measures
  • many beneficial effects of testosterone, including inhibition of proinflammatory cytokine expression
  • neuroprotection [80,81], are dependent upon androgen receptors, the observed effects of testosterone in this study may involve androgen receptor activation
  • testosterone can be converted by the enzyme aromatase into estradiol, which is also known to exert anti-inflammatory [82] and neuroprotective [83] actions
  • glia are the primary sources of proinflammatory molecules in the CNS
  • poorer survival of neurons grown on glia from mice maintained on high-fat diet
  • Since testosterone can affect glial function [86] and improve neuronal growth and survival [87–89], it was unexpected that testosterone status exhibited rather modest effects on neural health indices with the only significant response being an increase in survival in the testosterone-treated, high-fat diet group
  • significantly increased expression of TNFα and IL-1β in glia cultures derived from obese mice
  • testosterone treatment significantly lowered TNFα and IL-1β expression to near basal levels even in obese mice, indicating a protective benefit of testosterone across diet conditions
  • IL-1β treatment has been shown to induce synapse loss and inhibit differentiation of neurons
  • Testosterone status and diet-induced obesity were associated with significant regulation of macrophage infiltration
  • testosterone prevented and/or restored thermal nociception in both diet groups
  • a possible mechanism by which obesity and testosterone levels may affect the health of both CNS and PNS
  • Nathan Goodyear on 28 Apr 15
     
    Study points to obesity and low Testosterone contribution of neuroinflammation.  No effect of body weight was seen with TRT.  This animal model found similar positive effects of TRT in insulin sensitivity.  Obesity and low T increase inflammatory cytokine production: this study found an increase in TNF-alpha and IL-1beta and TRT reduced TNF-alpha and IL-1beta to near base-line.  Testosterone is neuroprotective and this study reviewed the small volume of evaded that pointed to benefit from estradiol.  Testosterone's effect on glial survival was positive but not significant.  Obesity and low T were found to be associated with increased macrophage infiltration in the PNS with increased TNF-alpha and IL-1beta.   Testosterone therapy improved peripheral neuropathy via its positive effects on nocicieption.
Nathan Goodyear

Testosterone supplementation in aging men and women: possible impact on cardiovascular-... - 0 views

ajprenal.physiology.org/...F941.full

low T low testosterone kidney kidneys therapy testosterone hormone hormones

shared by Nathan Goodyear on 05 Mar 13 - No Cached
  • Nathan Goodyear on 05 Mar 13
     
    This study proposes that testosterone therapy aids in renal dysfunction in men.  However, they document that IL-6 and TNF-alpha and oxidative stress are a part of this process. What they fail to mention is that aromatase activity and conversion of T to E in men increases IL-6 and TNF-alpha.  Studies have also shown that T decreases TNF-alpha. Very likely, it is high aromatase activity causing the effects documented by this study.
Nathan Goodyear

The Complex Role of Estrogens in Inflammation - 0 views

edrv.endojournals.org/...521.full

estrogens inflammation

shared by Nathan Goodyear on 14 Aug 12 - No Cached
  • These studies suggest inflammation-dependent up-regulation of ERβ relative to ERα.
  • up-regulation of ERβ relative to ERα under hypoxic conditions, which might lead to a preponderance of signaling through ERβ pathways
  • it seems that E2 at periovulatory to pregnancy levels inhibited proinflammatory cytokines from PBMCs
  • ...26 more annotations...
  • it is clear that E2 can stimulate antibody production by B cells, probably by inhibiting T cell suppression of B cells
  • In cycling women, the largest quantities of Ig were detected before ovulation
  • In contrast, E2 at high concentrations leads to a suppression of B-lymphocyte lineage precursors
  • E2 at periovulatory to pregnancy serum levels is able to stimulate antibody secretion under healthy conditions but also in autoimmune diseases, whereas similar serum levels of E2 lead to a suppression of bone marrow B cell lineage precursors
  • In chronic inflammatory disorders, where B cells play a decisive role, E2 would promote the disease when autoaggressive B cells are already present, whereas chronically elevated E2 would inhibit initiation of an autoimmune disease when no such B cells are available. This might be a good reason why particularly B cell-dependent diseases such as SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis appear in women in the reproductive years, predominantly, in the third or fourth decades of life
  • Th17 cells are thought to be the main responsible cells for chronic inflammatory tissue destruction in autoimmune diseases
  • IFN-γ, IL-12, and TNF were allocated to Th1 reactions
  • IL-4, IL-5, and IL-10 to Th2 responses
  • antiinflammatory T regulatory cells producing TGF-β and proinflammatory T helper type 17 cells (Th17) producing IL-17
  • no direct effects of estrogens on Th17 cells or IL-17 secretion have been described until now.
  • So-called Th17 cells producing IL-17 are the main T cells responsible for chronic inflammation.
  • Because IFN-γ has been allocated a Th17-inhibiting role (Fig. 1⇑), its increase by E2 at pregnancy doses and the E2-mediated inhibition of TNF must be viewed as a favorable effect in chronic inflammation
  • in humans and mice, E2 at periovulatory to pregnancy levels stimulates IL-4, IL-10, and IFN-γ but inhibits TNF from CD4+ T cells
  • In humans and mice, E3 and E2, respectively, at pregnancy levels inhibit T cell-dependent delayed type hypersensitivity
  • increased IL-4, IL-10, and IFN-γ in the presence of low TNF support an antiaggressive immune response
  • secretion of IL-1β is increased at periovulatory/proestrus to early pregnancy levels, whereas IL-1 secretion is inhibited at high pregnancy levels
  • The dichotomous effect of E2 on IL-1β and TNF at high and low concentrations is most probably due to inhibition of NF-κB at high concentrations
  • experiments with mouse and rat macroglial and microglial cells demonstrate that E2 at proestrus to pregnancy levels exerts neuroprotective effects by increasing TGF-β and by inhibiting iNOS and NO release, and reducing expression of proinflammatory cytokines and prostaglandin E2 production.
  • E2 at periovulatory to pregnancy levels inhibits NF-κB activation, which must be viewed as an antiinflammatory signal
  • It was shown that E2 concentrations equal to or above 10−10 m are necessary to inhibit NF-κB activation
  • important proinflammatory cytokines are typically inhibited at periovulatory (proestrus) to pregnancy levels of E2, which is evident for IL-6, IL-8, and TNF
  • low E2 concentrations were demonstrated to have no or even stimulatory effects
  • This renders a woman in the postmenopausal phase to a more proinflammatory situation
  • most in vitro studies demonstrated a stimulatory effect of E2 on secretion of IL-4, IL-10, and TGF-β typically at periovulatory to pregnancy levels
  • E2 at periovulatory to pregnancy levels has an ameliorating effect on chronic inflammatory diseases as long as B cell-dependent immunity or an overshooting fibrotic tissue repair process do not play a crucial pathogenic role. However, when the B cell plays an important role, E2 might even stimulate the disease process as substantiated by flare-ups in SLE during pregnancy
    • Nathan Goodyear
      Nathan Goodyear on 15 Aug 12
       
      SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis
  • Short-term administration of E2 at pregnancy levels was shown to induce an inflammatory response specific to the lateral prostate of the castrated male rat
  • Nathan Goodyear on 14 Aug 12
     
    great review of the complex interaction between Estrogens and inflammation.  Reference here is in females.
Nathan Goodyear

Inflammation in Response to Glucose Ingestion Is Independent of Excess Abdominal Adipos... - 0 views

jcem.endojournals.org/...4071.abstract

PCOS polycystic ovarian syndrome inflammation TNF-alpha CRP women androgens testosterone

shared by Nathan Goodyear on 09 Nov 12 - No Cached
  • Nathan Goodyear on 09 Nov 12
     
    women with PCOS, inflammatory cytokines TNF-alpha and CRP, associated with increasing androgen levels and with abdominal fat.  Women with less fat had lower levels of TNF-alpha and CRP than their higher weight counterparts, though the inflammatory cytokines were still evident.
Nathan Goodyear

Tumor necrosis factor-α and muscle wasting: a cellular perspective - 0 views

www.ncbi.nlm.nih.gov/...PMC59514

muscle loss wasting TNF-alpha inflammation

shared by Nathan Goodyear on 12 Nov 12 - No Cached
  • Nathan Goodyear on 12 Nov 12
     
    TNF-alpha associated with muscle loss and weakness.  TNF-alpha may also decrease testosterone production/secretion resulting in muscle loss.  
Nathan Goodyear

Inflammation and exercise: Inhibition of monocytic intracellular TNF producti... - 0 views

www.sciencedirect.com/...S0889159116305645

inflammation exercise TNF TNF-alpha

shared by Nathan Goodyear on 17 Jan 17 - No Cached
  • Nathan Goodyear on 17 Jan 17
     
    20 minutes of moderate exercise found to decrease inflammation, specifically TNF.
Nathan Goodyear

Antineoplastic Mechanisms of Niclosamide in Acute Myelogenous Leukemia Stem C... - 0 views

cancerres.aacrjournals.org/...2516

Niclosamide cancer leukemia NF-kappaB ROS TNF tumor necrosis factor

shared by Nathan Goodyear on 21 Mar 18 - No Cached
  • Here, we report on niclosamide as an antileukemic agent with two independent antineoplastic mechanisms: NF-κB pathway inactivation and ROS generation
  • In this report, we validated the inhibitory action of niclosamide against tumor necrosis factor (TNF)–induced NF-κB activation in AML cells and identified its mechanism, together with generation of reactive oxygen species (ROS), as being responsible for induced apoptosis of AML cells
  • NF-κB plays a critical role in inflammation, antiapoptotic responses, and carcinogenesis
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  • pharmacologic inhibition of NF-κB was effective in killing AML cells
  • High NF-κB expression is found in primitive human AML blast cells
  • niclosamide inhibited the TNF-induced NF-κB reporter activity in a dose- and time-dependent manner
  • niclosamide inhibiting TNF-induced IKK phosphorylation (Fig. 2A), niclosamide may exert its inhibitory effect at the TAK1 step
  • Pretreatment with niclosamide completely blocked the time- and dose-dependent TNFα-induced alteration of the NF-κB–DNA complex
  • niclosamide inhibited constitutively active NF-κB binding to DNA in U266 cells
  • niclosamide completely abolished the TNFα-induced phosphorylation of IKKα/β and IκBα
  • Accordingly, the TNFα-induced degradation of IκBα was abrogated by niclosamide
  • Nathan Goodyear on 21 Mar 18
     
    Old anti-parasitic medication, niclosamide, found to have anti-leukemic acitivty through inactivation of NF-kappaB and increase in ROS production in in Vitro and in Vivo study.
Nathan Goodyear

Modulation of tumor necrosis factor alpha expre... [Arch Toxicol. 1999] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...10650912

TNF-alpha TNF aluminum Al brain

shared by Nathan Goodyear on 26 Nov 13 - No Cached
  • Nathan Goodyear on 26 Nov 13
     
    mouse brain model found increased brain TNF alpha as a result of aluminum levels found in drinking water.
Nathan Goodyear

TNFR1-induced NF-κB, but not ERK, p38MAPK or JNK activation, mediates TNF-ind... - 0 views

www.sciencedirect.com/...S0898656807000198

TNF-alpha NF-kappaB ERK JNK p38MAPK inflammation

shared by Nathan Goodyear on 09 Oct 14 - No Cached
  • Nathan Goodyear on 09 Oct 14
     
    TNF-alpha stimulates NF-kappaB through non ERK, p38MAPK, and or JNK pathways.
Nathan Goodyear

Importance of TNF-alpha and leptin in obesity and ... [Exerc Immunol Rev. 1998] - PubMe... - 0 views

www.ncbi.nlm.nih.gov/...9644096

obesity leptin inflammation exercise

shared by Nathan Goodyear on 08 Mar 11 - No Cached
  • weight loss reduces adipose TNF-alpha expression and serum leptin levels and is associated with improved insulin sensitivity and lipid metabolism
  • Nathan Goodyear on 08 Mar 11
     
    weight loss reduces adipose inflammation signaling, TNF-alpha expression, and serum leptin levels and is associated with improved insulin sensitivity and lipid metabolism.
Nathan Goodyear

Alpha-lipoic acid inhibits TNF-alpha-induced NF-kapp... [FASEB J. 2001] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...11689467

Alpha-lipoic acid NF-kapppB TNF-alpha inflammation

shared by Nathan Goodyear on 06 Sep 11 - No Cached
  • Nathan Goodyear on 06 Sep 11
     
    alpha lipoic acid inhibits NF-kappa B activation by inhibiting TNF-alpha
Nathan Goodyear

Vitamin C Mitigates Oxidative Stress and Tumor Necrosis Factor-Alpha in Severe Communit... - 0 views

www.hindawi.com/...426740

LPS lipopolysaccharides ROS TNF-alpha TNF tumor necrosis factor IL-6 inflammation pneumonia vitamin C

shared by Nathan Goodyear on 06 Dec 17 - No Cached
  • Nathan Goodyear on 06 Dec 17
     
    Cell culture study found that vitamin C inhibited LPS mediated increase in ROS, TNF-alpha, IL-6... The cells were taken from adults with pneumonia
Nathan Goodyear

Activation of the hypothalamo-pituitary-a... [Intensive Care Med. 1999] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...10660848

TSH TSH suppression thyroid inflammation inflammatory cytokines IL-1Beta IL-6 TNF-alpha

shared by Nathan Goodyear on 01 Feb 13 - No Cached
  • Nathan Goodyear on 01 Feb 13
     
    Septic illnesses found to be associated with suppression of TSH centrally in the HPA axis. The cytokines found to be elevated were IL-1beta, TNF-alpha, and IL-6.
Nathan Goodyear

Suppression of Rat Thyrotroph and Thyroid Cell Function by Tumor Necrosis Factor-&#x3b1... - 0 views

online.liebertpub.com/...thy.1993.3.325

TNF-alpha inflammation inflammatory cytokines TSH TSH suppression thyroid

shared by Nathan Goodyear on 01 Feb 13 - No Cached
  • Nathan Goodyear on 01 Feb 13
     
    TNF-alpha inhibits TSH secretion in response to TRH stimulus.
Nathan Goodyear

Prolonged effects of tumor necrosis factor-alpha on... [Peptides. 1995] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...7479297

TSH TSH suppression TNF-alpha inflammation inflammatory cytokine thyroid

shared by Nathan Goodyear on 01 Feb 13 - No Cached
  • Nathan Goodyear on 01 Feb 13
     
    TNF-alpha shown to inhibit TSH release from the anterior pituitary.
Nathan Goodyear

Inflammatory responses to trivalent influenza virus ... [Vaccine. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21945263

influenza flu pregnancy CRP IL-6 TNF-alpha women preeclampsia preterm delivery PTD vaccine

shared by Nathan Goodyear on 07 Nov 12 - No Cached
  • Nathan Goodyear on 07 Nov 12
     
    This article's conclusion fits the definition of insane. This article found that the flu vaccine in pregnant women found significant increased CRP, TNF-alpha, and IL-6 inflammatory biomarkers.  It is well recognized the impact of inflammation on health and in this case the developing baby.   For example, preeclampsia and preterm birth are inflammatory conditions.  Yet, ACOG has made recommmendations for all pregnant women to get the flu vaccine?!?! Here is their conclusion: "However, further research is needed to confirm that the mild inflammatory response elicited by vaccination is benign in pregnancy".  Take home, you are being studied to see the effects of the flu vaccine on you, if you are pregnant, and your developing child.  And who decides what "mild" is anyways.  If you develop preeclampsia and delivery early, where is the "mild" in that?
Nathan Goodyear

Biology of Cachexia - 0 views

jnci.oxfordjournals.org/...1763.full

cachexia cancer metabolism TNF-alpha IL-1 IL-6

shared by Nathan Goodyear on 03 Jul 13 - No Cached
  • Nathan Goodyear on 03 Jul 13
     
    Another good review on the metabolism of cancer.  But, this article touches on the cachexia effects from cancer.  Inflammatory cytokines TNF-alpha, IL-1, IL-6 play role in these decreased appetite and weight loss symptoms.
Nathan Goodyear

C-Reactive Protein in Healthy Subjects: Associations With Obesity, Insulin Resistance, ... - 0 views

atvb.ahajournals.org/...972.full

inflammation insulin resistance obesity GLUT4 receptor IL-1B TNF-alpha NF-KappaB

shared by Nathan Goodyear on 17 Oct 12 - No Cached
  • Nathan Goodyear on 17 Oct 12
     
    The summary statement of this article says it all: "chronic inflammatory state may induce insulin resistance and endothelial dysfunction..."  Inflammation causes insulin dysfunction. And in fact, we know this to be true.  We know that IL-1B and TNF-alpha stimulated by NF-KappaB actually inhibits insulin action via disruption of the GLUT4 receptor.
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