Exercise And IL-6 Infusion Inhibit Endotoxin-induced TNF-α P

Edward

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Exercise and IL-6 infusion inhibit endotoxin-induced TNF-α production in humans
http://www.fasebj.org/content/17/8/884.full

"We hypothesized that IL-6 acts to decrease the production of TNF-α, and given that IL-6 is produced during physical exercise, we further suggested that exercise inhibits TNF production. Thus, the aim of the present study was to determine whether rhIL-6 infusion and physical exercise would inhibit the production of TNF induced by low-grade endotoxemia in humans."

Probably a garden would do.
 

Dan Wich

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Re: Exercise and IL-6 infusion inhibit endotoxin-induced TNF

Thanks for this, I'd like to lower TNF-a levels based on wild speculation that it will help trigger point problems. Though I don't even know if I have high levels, and even if I do, whether they're from endotoxin.

Edward said:
Probably a garden would do.
I hope you're right, 3 hours on a bicycle at 75% VO2 max would not be pleasant.
 

Edward

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Re: Exercise and IL-6 infusion inhibit endotoxin-induced TNF

Glycine suppresses TNF-α-induced activation of NF-κB in differentiated 3T3-L1 adipocytes
http://www.ncbi.nlm.nih.gov/pubmed/22732655

Glycine strongly reduces the serum levels of pro-inflammatory cytokines and increases the levels of anti-inflammatory cytokines. Recently, glycine has been shown to decrease the expression and secretion of pro-inflammatory adipokines in monosodium glutamate-induced obese (MSG/Ob) mice. It has been postulated that these effects may be explained by a reduction in nuclear factor kappa B (NF-κB) activation. NF-κB is a transcription factor, which is crucial to the inflammatory response. Hasegawa et al. (2011 and 2012) recently reported a glycine-dependent reduction in NF-κB levels. Here, we have investigated the role of glycine in the regulation of NF-κB in differentiated 3T3-L1 adipocytes. The results revealed that pretreatment with glycine interfered with the activation of NF-κB, which has been shown to be stimulated by tumor necrosis factor-alpha (TNF-α). Glycine alone stimulated NF-κB activation in an unusual way such that the inhibitor κB-β (IκB-β) degradation was more significant than that of the inhibitor κB-α (IκB-α) and led to NF-κB complexes comprised of p50 and p65 subunits; IκB-ε degradation did not affect by glycine. These findings suggest that glycine could be used as an alternative treatment for chronic inflammation, which is a hallmark of obesity and other comorbidities, and is characterized by an elevated production of pro-inflammatory cytokines.

I used to have really bad trigger points/muscle knots especially in the rotator cuff area and in that region in general... one thing fixed it and I haven't had a problem since, Cynoplus, because it modulates calcium channeling among other things (but the calcium channeling is more relevant here) and specifically the T4 component because T4 lowers TSH which is inflammatory.

Dr. Peat said:
It (T4) lowers TSH, which is inflammatory, and is responsible for some of the important symptoms of hypothyroidism.
 

NathanK

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Good stuff. As mentioned in Haidut's addiction podcast this week. So glycine and exercise can lower inflammatory cytokines. It looks like TNF-a is dircectly caused by endotoxin/LPS and can lead to insulin resistance

From FPS:
Trends Endocrinol Metab. 2000 Aug;11(6):212-7.
Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes.d
Moller DE.
Tumor necrosis factor alpha (TNF-alpha) has well-described effects on lipid metabolism in the context of acute inflammation, as in sepsis. Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. Multiple mechanisms have been suggested to account for these metabolic effects of TNF-alpha. These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia.
 
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