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jemini

Sesamin for acne?

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Well the topic says it all pretty much. I was wondering if anyone has ever taken sesamin for acne. Sesamin is supposedly a ppar agonist which was supposed to help people lose weight by making you metabolize fat. People on bodybuilding websites say it didn't really help them lose much fat, but many do claim it did help clear their skin. One on the cutting edge areas of acne research involves dgat's and ppars. I was wondering if anyone could enlighten me on the subject or their experience with sesamin.

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Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital Box 232, Hills Road, Cambridge CB2 2QR, UK. [email protected]

BACKGROUND: Nuclear hormone receptors are important in the regulation of epidermal differentiation and have been implicated in lipid metabolism. In particular, there is evidence suggesting that the activation of peroxisome proliferator-activated receptors (PPARs) is an important factor in the regulation of sebocyte lipogenesis. OBJECTIVES: To determine the role of PPARs, farnesoid X receptor (FXR) and other orphan nuclear hormone receptors in sebaceous gland function in vitro by investigating the biochemical effects of appropriate ligands, and by establishing the RNA and protein expression patterns of a number of nuclear receptors in sebaceous glands ex vivo. METHODS: Human chest sebaceous glands were maintained in vitro as freshly isolated and as 7-day cultured whole organs. We then studied the effects of appropriate ligands on the glandular rates of lipogenesis and DNA synthesis, as well as determining the mRNA (reverse transcription-polymerase chain reaction) and protein expression patterns (immunohistochemistry/immunoblotting) of the nuclear hormone receptors of interest. RESULTS: PPAR ligands, but not FXR ligands, inhibited sebaceous lipogenesis, in particular the PPARalpha ligands LY 171883 and WY 14643, and the PPARgamma ligands BRL 49653 and 15-deoxy-Delta-12,14-prostaglandin J(2). We detected RNA expression of PPARalpha, PPARbeta, PPARgamma, retinoid X receptor alpha, liver X receptor alpha (LXRalpha) and pregnane X receptor but not FXR in freshly isolated and 7-day maintained sebaceous glands. PPARalpha, PPARbeta, PPARgamma and LXRalpha protein were detected in nuclear extracts of sebaceous glands. CONCLUSIONS: We conclude that activation of nuclear hormone receptors, in particular activation of PPARalpha and PPARgamma, can regulate lipogenesis in human sebaceous glands. As suppression of sebum secretion is associated with reduced acne activity, the nuclear hormone receptors involved may open new avenues in the development of novel acne treatments.

Sesamin is a ppar ALPHA agonist. After doing a little research the jury is still out as to what effect these different ligands have. I found one study which said that agonists for ANY of the ppars (alpha beta/delta or gamma) increased sebum output. This one implies they have some sort of feedback on each, so by increasing expression of one you decrease the expression of the others. Since Alpha is not really the major player in sebum production, the added sebum produced by activating alpha may not compare to the overall reduction of sebum by blocking beta/delta and gamma.

PPAR-beta/delta - 95%

PPARgamma - 66%

PPARalpha - 20%

PPARgamma + DHT = 70%

DHT = 25%

Control = 11%

http://www.ncbi.nlm.nih.gov/entrez/query.f...st_uids=9557223

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I ordered some sesamin to give this theory a try. I wonder how powerful of an alpha agonist this extract is and how strong its effects on sebum production are. There are some anecdotal claims on bodybuilding boards that the reason it might help skin is that sesamin is estrogenic. There was a study on menapausal women which hinted at this effect. But the study was vague at best. It involved eating high doses of raw sesame seeds, not the extract and the study only looked at a narrow range of subjects. Some bodybuillders claimed it made them feel tired and gave their muscles a flat look, which would be typical of estrogen. But they were taking high doses of the stuff usually 2+ caps a day. I think 1 cap of extract should be plenty potent. My hypothesis is that by itself, sesamin probably isn't going to get rid of acne. But if it does reduce excess oil significantly, it could be a nice addition to a prexisting regimen.

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Here is a conflicting study though

Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPARα agonist-GW7647, PPARδ agonist-GW0742, PPARα/δ agonist-GW2433, PPARγ agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.

This basically says that activation of any of the ppar's caused An increase in sebum production. At first I thought I was misinterpreting the first study and the ligands used were antagonists. But then I googled both ly 171883 and wy 14643 and both turned out to be PPAR agonists. So these studies have opposite conclusions.

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Wow, there is tons of cutting edge research about this stuff and its relation to acne. Here is an intereting snippet from http://www.nature.com/jid/journal/v125/n5/full/5603596a.html

proliferation of the mouse preputial gland cells was also enhanced significantly by cPGI2. Interestingly, AA induces accumulation of lipids in human sebaceous gland cells in vitro (Wróbel et al, 2003) and downregulation PPAR-alpha through selective ligands has currently been suggested to be involved in the development of seborrhea and acne

Perhaps a ppar alpha agonist (sesamin) would help?

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i was really into all this stuff about three months ago but youre best bet may be with fish oil

The ligands for the PPARs are free fatty acids and eicosanoids. PPARγ is activated by PGJ2 (a prostaglandin). In contrast, PPARα is activated by leukotriene B4.

http://en.wikipedia.org/wiki/PPAR

eicosanoids are made from essential fatty acids

http://en.wikipedia.org/wiki/Image:EFA_to_Eicosanoids.svg

http://en.wikipedia.org/wiki/Eicosanoid

fish oil may have been the only supplement ive ever tried that actually made difference in my condition at first it cleared me completly for three weeks then for whatever reason the benefits kind of leveled off a bit. so from there i chose accutane since ive honestly tried everything worthwhile that actually had science to back it up, wasnt about to do anything without real evidence to back it up. Fish oil makes sense in so many ways for helping a condition like acne, helps inflammation, increases collagen production, down regulates

cox-2 and from epa forms the eicosanoid that binds to ppar and then to rxr receptor.

For people with very mild acne fish oil would probably work really well but if your acnes bad it will improve it quite a bit but of course its no cure.

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I currently take 2 grams of flax oil plus a spoonful in my yogurt and I haven't noticed a change in acne, been takin it for months too. I really just want to explore and test my options before hopping on accutane. I've taken it once and it works well, but I'm an adult which means accutane will just buy me some time before I begin to break out again. Anyway, I'm not saying sesamin is a cure all, but there are a good deal of claims where it has worked for acne. I'm just wondering exactly how potent the effects were, and if it was due to the ppar alpha agonism or its supposed estrogenlike effects. Have you tried sesamin?

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I currently take 2 grams of flax oil plus a spoonful in my yogurt and I haven't noticed a change in acne, been takin it for months too. I really just want to explore and test my options before hopping on accutane. I've taken it once and it works well, but I'm an adult which means accutane will just buy me some time before I begin to break out again. Anyway, I'm not saying sesamin is a cure all, but there are a good deal of claims where it has worked for acne. I'm just wondering exactly how potent the effects were, and if it was due to the ppar alpha agonism or its supposed estrogenlike effects. Have you tried sesamin?
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It didn't. It works much like fish oil, so if you had good results with fish oil, this might be a decent substitute since you wouldn't need to pop as many pills perhaps. I'm going on accutane this week.

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check this out.

Br J Dermatol. 2004 Oct;151(4):766-75. Links

Peroxisome proliferator-activated receptor and farnesoid X receptor ligands differentially regulate sebaceous differentiation in human sebaceous gland organ cultures in vitro.Downie MM, Sanders DA, Maier LM, Stock DM, Kealey T.

Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital Box 232, Hills Road, Cambridge CB2 2QR, UK. [email protected]

BACKGROUND: Nuclear hormone receptors are important in the regulation of epidermal differentiation and have been implicated in lipid metabolism. In particular, there is evidence suggesting that the activation of peroxisome proliferator-activated receptors (PPARs) is an important factor in the regulation of sebocyte lipogenesis. OBJECTIVES: To determine the role of PPARs, farnesoid X receptor (FXR) and other orphan nuclear hormone receptors in sebaceous gland function in vitro by investigating the biochemical effects of appropriate ligands, and by establishing the RNA and protein expression patterns of a number of nuclear receptors in sebaceous glands ex vivo. METHODS: Human chest sebaceous glands were maintained in vitro as freshly isolated and as 7-day cultured whole organs. We then studied the effects of appropriate ligands on the glandular rates of lipogenesis and DNA synthesis, as well as determining the mRNA (reverse transcription-polymerase chain reaction) and protein expression patterns (immunohistochemistry/immunoblotting) of the nuclear hormone receptors of interest. RESULTS: PPAR ligands, but not FXR ligands, inhibited sebaceous lipogenesis, in particular the PPARalpha ligands LY 171883 and WY 14643, and the PPARgamma ligands BRL 49653 and 15-deoxy-Delta-12,14-prostaglandin J(2). We detected RNA expression of PPARalpha, PPARbeta, PPARgamma, retinoid X receptor alpha, liver X receptor alpha (LXRalpha) and pregnane X receptor but not FXR in freshly isolated and 7-day maintained sebaceous glands. PPARalpha, PPARbeta, PPARgamma and LXRalpha protein were detected in nuclear extracts of sebaceous glands. CONCLUSIONS: We conclude that activation of nuclear hormone receptors, in particular activation of PPARalpha and PPARgamma, can regulate lipogenesis in human sebaceous glands. As suppression of sebum secretion is associated with reduced acne activity, the nuclear hormone receptors involved may open new avenues in the development of novel acne treatments.

Phytol directly activates peroxisome proliferator-activated receptor alpha (PPARalpha) and regulates gene expression involved in lipid metabolism in PPARalpha-expressing HepG2 hepatocytes.Goto T, Takahashi N, Kato S, Egawa K, Ebisu S, Moriyama T, Fushiki T, Kawada T.

Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji, Japan.

The peroxisome proliferator-activated receptor (PPAR) is one of the indispensable transcription factors for regulating lipid metabolism in various tissues. In our screening for natural compounds that activate PPAR using luciferase assays, a branched-carbon-chain alcohol (a component of chlorophylls), phytol, has been identified as a PPARalpha-specific activator. Phytol induced the increase in PPARalpha-dependent luciferase activity and the degree of in vitro binding of a coactivator, SRC-1, to GST-PPARalpha. Moreover, the addition of phytol upregulated the expression of PPARalpha-target genes at both mRNA and protein levels in PPARalpha-expressing HepG2 hepatocytes. These findings indicate that phytol is functional as a PPARalpha ligand and that it stimulates the expression of PPARalpha-target genes in intact cells. Because PPARalpha activation enhances circulating lipid clearance, phytol may be important in managing abnormalities in lipid metabolism.

So yea chlorophyll is the green pigment in leaves of plants, so when was the last time you ate a salad? I probably eat a salad about 4 times a year.

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I've seen most of that research. Here is what confuses me, the ligands in the first study are ANTAGONIST ligands. Which means they bind to the ppars but prevent them from turning on. Sesamin and fish oil are ppar alpha agonists, at least indirectly. which means they turn ppar alpha on so to speak. After doing some research and I could be wrong, the best way I can figure why sesamin and fish oil clear acne in some cases despite their ppar agonism is that through some mechanism, either through competing for key enzymes or something else that they inhibit ppar gamma. ppar gamma tends to be associated with an inflammation response, and gets activated indirectly by arachadonic (sp?) acid and inflammatory leukotrienes. That might explain when people take fish oil, they can notice either an increase in oil since it activates ppar alpha, or a decrease in oil by inhibiting the ligands for ppar gamma. My guess is it all really comes down to what is really causing your acne in the first place.

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I've seen most of that research. Here is what confuses me, the ligands in the first study are ANTAGONIST ligands. Which means they bind to the ppars but prevent them from turning on. Sesamin and fish oil are ppar alpha agonists, at least indirectly. which means they turn ppar alpha on so to speak. After doing some research and I could be wrong, the best way I can figure why sesamin and fish oil clear acne in some cases despite their ppar agonism is that through some mechanism, either through competing for key enzymes or something else that they inhibit ppar gamma. ppar gamma tends to be associated with an inflammation response, and gets activated indirectly by arachadonic (sp?) acid and inflammatory leukotrienes. That might explain when people take fish oil, they can notice either an increase in oil since it activates ppar alpha, or a decrease in oil by inhibiting the ligands for ppar gamma. My guess is it all really comes down to what is really causing your acne in the first place.
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I'm sorry, I googled some of the experimental compounds used in the experiment. Most were agonists, but LY 171883 is an antagonist. I also know there are conflicting studies about this stuff.

Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPAR agonist-GW7647, PPAR agonist-GW0742, PPAR/ agonist-GW2433, PPAR agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.

As far as I can tell, the research is so new and no one really knows how ppars work together. PPAR's are likely to be good candidates for future acne medicine, but it might not be as simple as an on/off switch.

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I'm sorry, I googled some of the experimental compounds used in the experiment. Most were agonists, but LY 171883 is an antagonist. I also know there are conflicting studies about this stuff.

Sebum production is key in the pathophysiology of acne, an extremely common condition, which when severe, may require treatment with isotretinoin, a known teratogen. Apart from isotretinoin and hormonal therapy, no agents are available to reduce sebum. Increasing our understanding of the regulation of sebum production is a milestone in identifying alternative therapeutic targets. Studies in sebocytes and human sebaceous glands indicate that agonists of peroxisome proliferator-activated receptors (PPARs) alter sebaceous lipid production. The goal of this study is to verify the expression and activity of PPARs in human skin and SEB-1 sebocytes and to assess the effects of PPAR ligands on sebum production in patients. To investigate the contribution of each receptor subtype to sebum production, lipogenesis assays were performed in SEB-1 sebocytes that were treated with PPAR ligands and isotretinoin. Isotretinoin significantly decreased lipogenesis, while the PPAR agonist-GW7647, PPAR agonist-GW0742, PPAR/ agonist-GW2433, PPAR agonist rosiglitazone, and the pan-agonist-GW4148, increased lipogenesis. Patients treated with thiazolidinediones or fibrates had significant increases in sebum production (37 and 77%, respectively) when compared to age-, disease-, and sex-matched controls. These data indicate that PPARs play a role in regulating sebum production and that selective modulation of their activity may represent a novel therapeutic strategy for the treatment of acne.

As far as I can tell, the research is so new and no one really knows how ppars work together. PPAR's are likely to be good candidates for future acne medicine, but it might not be as simple as an on/off switch.

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