Read on Twitter
Susceptibility to sunburns on high n-6 diets:
"UVB and H2O2 induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. [This] suggests that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions."
![Susceptibility to sunburns on high n-6 diets:"UVB and H2O2 induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. [This] suggests that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions."](https://pbs.twimg.com/media/EtrmGnkXcAAnmTE.jpg "Susceptibility to sunburns on high n-6 diets:\"UVB and H2O2 induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. [This] suggests that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions.\"")
"UVB and H2O2 induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. [This] suggests that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions."
G2A Plays Proinflammatory Roles in Human Keratinocytes under Oxidative Stress as a Receptor for 9-Hydroxyoctadecadienoic Acid
https://www.sciencedirect.com/science/article/pii/S0022202X15338549
#lcl6
https://www.sciencedirect.com/science/article/pii/S0022202X15338549
#lcl6
Why is epidermis rich in LA that is unstable and inflammatory under UVB?
How does diet influence lipid composition of skin?
How does diet influence lipid composition of skin?
Experience with resistance to sunburns after switching to low n-6 diet is very often, at least in my social bubble. Illustrative story:
http://yelling-stop.blogspot.com/2010/12/my-vitamin-d-experiment.html
http://yelling-stop.blogspot.com/2010/12/my-vitamin-d-experiment.html
More on G2A and 9-HODE
"The Lipid Receptor G2A (GPR132) Mediates Macrophage Migration in Nerve Injury-Induced Neuropathic Pain"
https://pubmed.ncbi.nlm.nih.gov/32708184
"Inhibiting the G2A receptor after nerve injury may reduce immune [response] and may thus ameliorate neuropathic pain."
"The Lipid Receptor G2A (GPR132) Mediates Macrophage Migration in Nerve Injury-Induced Neuropathic Pain"
https://pubmed.ncbi.nlm.nih.gov/32708184
"Inhibiting the G2A receptor after nerve injury may reduce immune [response] and may thus ameliorate neuropathic pain."
... and more:
"We discuss the underlying molecular mechanisms of the oxidizedkinokeic acid metabolites and eicosanoids. We evaluate their role as potential targets for the development of novel analgesics..."
Oxidized Lipids in Persistent Pain States https://www.frontiersin.org/articles/10.3389/fphar.2019.01147/full
"We discuss the underlying molecular mechanisms of the oxidizedkinokeic acid metabolites and eicosanoids. We evaluate their role as potential targets for the development of novel analgesics..."
Oxidized Lipids in Persistent Pain States https://www.frontiersin.org/articles/10.3389/fphar.2019.01147/full
Note to self (from previous paper): "Linoleic acid is one of the essential ω-6 fatty acids, which leads to formation of the smooth, non-dry outer epidermal barrier upon dietary intake (Hansen et al., 1958; Gill and Valivety, 1997; Nakamura and Nara, 2003; Ramsden et al., 2017)."
It makes sense to me that upstream metabolites of toxic compounds were evolutionary selected as messengers for pain and inflammation.
https://www.frontiersin.org/files/Articles/473908/fphar-10-01147-HTML/image_m/fphar-10-01147-t001b.jpg
https://www.frontiersin.org/files/Articles/473908/fphar-10-01147-HTML/image_m/fphar-10-01147-t001b.jpg
OXLAMs and psoriasis:
Bioactive Lipid Mediator Profiles in Human Psoriasis Skin and Blood
https://pubmed.ncbi.nlm.nih.gov/29454560/
Bioactive Lipid Mediator Profiles in Human Psoriasis Skin and Blood
https://pubmed.ncbi.nlm.nih.gov/29454560/
All papers in the thread cite the paper from the first tweet.
