Prolonged Niacin Treatment Leads To Increased Adipose Tissue Polyunsaturated Fatty Acid Synthesis

Peater Piper

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This regards niacin. I don't know if would also apply to niacinamide, hence posting it here to get opinions.

The gene expression profile of gonadal white adipose tissue (gWAT) from niacin treated mice showed an up-regulation of the “biosynthesis of poly unsaturated fatty acid (PUFA)” pathway, which was corroborated by qPCR and analysis of the FA ratios in gWAT. Also, adipocytes from niacin treated mice secreted more of the PUFA docosahexaenoic acid (DHA) ex vivo. This resulted in an increased DHA/arachidonic acid (AA) ratio in the adipocyte FA secretion profile and in plasma of niacin treated mice. Interestingly, the DHA metabolite 19,20-dihydroxy docosapentaenoic acid (19,20-diHDPA) was increased in plasma of niacin treated mice. Both an increased DHA/AA ratio and increased 19,20-diHDPA are indicative for an anti-inflammatory profile and may indirectly contribute to the atheroprotective lipid and lipoprotein profile associated with prolonged niacin treatment.

The current study demonstrates for the first time that prolonged niacin treatment results in an upregulation of the n-3 PUFA synthesis pathway in adipose tissue. Gene expression analysis of gWAT showed that our hyperlipidemic mouse model responded to niacin by up-regulating genes involved in the unsaturated FA biosynthesis. Fatty acid composition analysis corroborated the increased PUFA synthesis. A higher degree of n-3 PUFA secretion from prolonged niacin treated adipocytes was seen, which was also reflected in increased n-3 PUFA plasma levels. Markedly, the plasma levels of n-3 PUFA derived oxylipins produced by cytochrome P450 and hydrolyzed by soluble epoxy hydrolases were increased. Oxylipins produced by cytochrome P450 from n-3 PUFAs and the n-3 PUFAs themselves suggest a beneficial vascular health profile, which might contribute to the prolonged niacin-induced atheroprotective effect.

http://www.jlr.org/content/early/2014/10/15/jlr.M051938.full.pdf
 

Peater Piper

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Some more studies, this time using nicotinamide.

In the first, a 100 mg dose of nicotinamide in human volunteers caused a rise in plasma levels of histamine and serotonin. Considering most Peaters are trying to lower both histamine and serotonin, and also get good results with nicotinamide, I'm not sure what to make of a low(ish) dose of nicotinamide causing them to increase.
Excess nicotinamide increases plasma serotonin and histamine levels. - PubMed - NCBI

In the second study, 100 mg of nicotinamide caused a rise in homocysteine, possibly by depleting methyl donors. I know Peat isn't fond of methylation, but the rise in homocysteine is a little concerning. Thoughts?
Excess nicotinamide inhibits methylation-mediated degradation of catecholamines in normotensives and hypertensives. - PubMed - NCBI
 

Peater Piper

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I don't think this would apply to humans, since we can't synthesize the Omega 3 or 6 fatty acids. That's why they are "essential."
That's a trait of all mammals, as far as I'm aware. I assumed the study was showing increased synthesis of DHA from a-linoleic acid. In humans, very little ALA is converted to DHA and EPA. Increased conversion would mean taking an already volatile fatty acid and making it more prone to oxidation, although considering the minute amounts of omega 3's in a Peat diet it may not matter. Plus, I don't know if niacinamide would cause the same result as niacin.
 

judge

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atheroprotective lipid and lipoprotein profile associated with prolonged niacin treatment. FYI that is a GOOD thing!
 
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