Glucosamine (glycolysis inhibitor) extends lifespan?

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overkees
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Glucosamine (glycolysis inhibitor) extends lifespan?

Post by overkees »

http://www.nature.com/ncomms/2014/14040 ... s4563.html

In this article it states that Glucosamine extends lifespan of ageing mice and nematodes by increasing ROS and inhibiting glycolysis, they conclude that it is therefore mimicking a low carb diet.

They further say
Mitochondrial ROS signalling in nematodes and, in particular, mitohormesis suggests that a low-dose, transient increase in ROS formation promotes metabolic health and life span, thereby questioning the free radical theory of ageing. To test whether the increase in ROS is essential for a GlcN-mediated extension of life span, we repeated the initial life span experiment in the presence of the antioxidants butylated hydroxyl anisole (BHA) and N-acetyl-cystein (NAC), respectively. Although neither BHA nor NAC had a detectable effect on C. elegans life span in the absence of GlcN, the life span-extending capabilities of GlcN were nullified in the presence of BHA or NAC. This indicates that the transient increase in ROS is required for the extension of life span caused by GlcN, thus providing additional support for adaptive ROS signalling or mitohormesis or both.
This is debatable since BHA is a known carcinogen and can in fact under certain conditions be a pro-oxidant. Cystein is, correct me if I'm wrong, an inhibitor of autophagy?

My reasoning would be that ageing rodents have a buildup of toxins and mutations in their body and inhibiting glycolysis might emphasize the autophagy cycle and extent lifespan for this reason. But I'm not quite sure yet. Can anybody see some other mechanisms at play with the perspective of autophagy or ROS reduction extending lifespan? RRM?
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RRM
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Re: Glucosamine (glycolysis inhibitor) extends lifespan?

Post by RRM »

overkees wrote:In this article it states that Glucosamine extends lifespan of ageing mice and nematodes by increasing ROS and inhibiting glycolysis, they conclude that it is therefore mimicking a low carb diet.
Glycation of proteins and nucleotides results in AGEs/ALEs, which are associated to ageing. Its the cells structures (incl. DNA/RNA) that get compromised.
Autophagy cleans up damage like that.
Glycation of proteins and nucleotides is caused by glycolytic intermediates, most notably alpha-oxoaldehydes.
They don't just result from sugars, protein and fats endogenously, but are also taken up in the blood by consuming cooked foods.
This is explained on the Maillard reaction wiki page.
http://www.waiwiki.org/index.php?title= ... d_reaction
Cystein is, correct me if I'm wrong, an inhibitor of autophagy?
Yes, protein (levels) is.
But on the other hand acetylcysteine (and taurine) is derived from cysteine, and is a precursor in the formation of glutathione. Cysteine (binds to aldehydes) and glutathione inhibit the Maillard reaction more so than citric acid and oxalic acid. Taurine also inhibits AGE formation.
inhibiting glycolysis might emphasize the autophagy cycle and extent lifespan for this reason.
Many substances inhibit glycolysis, or counteract the results.
http://www.waiwiki.org/index.php?title= ... Inhibitors
Autophagy cleans up the damage caused by the end products.
Can anybody see some other mechanisms at play with the perspective of autophagy or ROS reduction extending lifespan? RRM?
That ROS reduction extends lifespan has appeared to be an outdated theory, and is also shown by the study you quoted.
Recent studies have shown that its actually autophagy.
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