NLRP3 as a mediator of inflammation

Pdohlen

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The NLRP3 Inflammasome as a Novel Player of the Intercellular Crosstalk in Metabolic Disorders/

Interesting research article pointing at NLRP3 as a mediator of inflammation:

High fat diets was mentioned as an activator.

"In vitro experiments have shown that elevated concentration of saturated fatty acids (SFAs), caused by a high-fat diet, may activate the NLRP3 inflammasome in macrophages through a newly identified AMP-activated protein kinase and unc-51-like kinase-1 autophagy signaling cascade [13]. Besides, both ex vivo and in vivo exposure of bone marrow derived dendritic cells to dietary SFA resulted in increased NLRP3 inflammasome activation and reduced adipocyte insulin sensitivity. More specifically, dietary SFA may act as a primer of the NLRP3 inflammasome protein complex enhancing NLRP3, caspase-1, and pro-IL-1β mRNA expression."

High Fructose syrup raises Uric Acid, which activate NLRP3 inflammasone. (What about sugar?)

"In an animal study aimed to evaluate the renal consequences of the chronic administration of high-fructose corn syrup (HFCS-55), the major sweetener in foods and soft-drinks, we have recently demonstrated that HFCS-55 feeding caused a significant increase in body weight and more importantly dyslipidemia, hyperinsulinemia, and an increase in insulin resistance due to impaired insulin signaling [60]. Most notably, the HFCS-55 diet evoked upregulation of renal NLRP3 expression, resulting in activation of caspase-1 and the subsequent cleavage of pro-IL1β to the biologically active secreted form IL-1β. These effects were due, at least in part, to the marked hyperuricemia afforded by the dietary manipulation, as also confirmed by a previous study demonstrating that increased levels of uric acid directly activate the NLRP3 inflammasome [61]. Similarly, rats fed with fructose, which is known to raise uric acid levels, showed a significant increase in renal protein levels of NLRP3 [62]."

Also found it interesting that D3 was highlighted as an other culprit?

"Zhou et al. [39] were the first to identify a possible signaling pathway involved in NLRP3 inflammasome activation under conditions of metabolic stress. They showed that thioredoxin-interacting protein (TXNIP), also known as vitamin D3 upregulated protein 1 (VDUP1), is an upstream and highly selective activating ligand for NLRP3, with no effect on the activity of other inflammasomes (e.g., NLRC4 and AIM2). TXNIP-dependent NLRP3 inflammasome activation drives IL-1β secretion from pancreatic islets in response to chronic elevated glucose, thus suggesting, for the first time, that NLRP3, activated under conditions of metabolic stress, mediates IL-1β-driven islet failure."
 

LeeLemonoil

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Fits in nicely with Panbeckers thinking that inhibited autophagy leads to Nlrp3-overactivity.
 

Perry Staltic

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keytothecity

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new chemhead replies, dare I say they are interesting

he also started replying here




@LeeLemonoil
@GorillaHead
 

keytothecity

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new chemhead replies, dare I say they are interesting

he also started replying here




@LeeLemonoil
@GorillaHead
Woops wrong thread ima copy this to the right one
 

Scenes

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Woops wrong thread ima copy this to the right one
By this logic, dhea topical should be great for hair. Provides necessary androgens and allows estrogen in conversion as necessary. Chemhead seems to suggest dht is bad because it removes the possibility of estrogenisation in the follicles.
 

keytothecity

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By this logic, dhea topical should be great for hair. Provides necessary androgens and allows estrogen in conversion as necessary. Chemhead seems to suggest dht is bad because it removes the possibility of estrogenisation in the follicles.
I don't think he believes in topicals due to lack of osmotic pressure (if I remember correctly) to get the estrogen there. It's somewhere in his newer posts. You need full blown feminizitation to make E work according to him.
 

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