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Dashforce posted this over on M&M and I looked into pricing out TUDCA and PBA but latter is quite expensive and the former is only available in Liver Longer,which is not all that pricey but discontinued.If these two,or even just TUDCA but preferably both,could be sourced in bulk,I'm sure that it would sell.I'd be down for a pre-order/pre-payment if price was decent.TUDCA is the active in Liver Longer so that should be pretty affordable in bulk but PBA was top dollar but given D Sade's sourcing talents,maybe RPN can set something up?
Those interested,please post.
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[quote name='dashforce' date='Apr 14 2009, 11:56 AM' post='544828']
C&P from Bachovas' "Abstracts and Studies" thread
An article in MD led me to find this one... the taurourodeoxycholic acid is just a bile acid, normally produced in humans (and thus likely non-toxic). Taurine may help bile acid conjugation, I wonder if it increases this chemical...
Buphenyl (the other one, may have spelled that wrong) is also available for human use in the treatment of urea cycle disorders, but it's recommended only in conjunction with a low PRO diet...
According to the MD article, up to a 10X increase in leptin sensitivity was seen... but it didn't say which drug that was due to. But that's pretty amazing... I imagine if it works as well in lean humans as in obese mice, you could chill at 6% bf all year round feeling like a champ and eating however you want.
In fact I think I'll make this a new thread...
[/quote]
Cell Metab. 2009 Jan 7;9(1):35-51. Links
Endoplasmic reticulum stress plays a central role in development of leptin resistance.
Ozcan L, Ergin AS, Lu A, Chung J, Sarkar S, Nie D, Myers MG Jr, Ozcan U.
Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA.
Leptin has not evolved as a therapeutic modality for the treatment of obesity due to the prevalence of leptin resistance in a majority of the obese population. Nevertheless, the molecular mechanisms of leptin resistance remain poorly understood. Here, we show that increased endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) in the hypothalamus of obese mice inhibits leptin receptor signaling. The genetic imposition of reduced ER capacity in mice results in severe leptin resistance and leads to a significant augmentation of obesity on a high-fat diet. Moreover, we show that chemical chaperones, 4-phenyl butyric acid (PBA), and tauroursodeoxycholic acid (TUDCA), which have the ability to decrease ER stress, act as leptin-sensitizing agents. Taken together, our results may provide the basis for a novel treatment of obesity.
PMID: 19117545 [PubMed - indexed for MEDLINE]
Full article:
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Those interested,please post.
Invalid Link Removed
[quote name='dashforce' date='Apr 14 2009, 11:56 AM' post='544828']
C&P from Bachovas' "Abstracts and Studies" thread
An article in MD led me to find this one... the taurourodeoxycholic acid is just a bile acid, normally produced in humans (and thus likely non-toxic). Taurine may help bile acid conjugation, I wonder if it increases this chemical...
Buphenyl (the other one, may have spelled that wrong) is also available for human use in the treatment of urea cycle disorders, but it's recommended only in conjunction with a low PRO diet...
According to the MD article, up to a 10X increase in leptin sensitivity was seen... but it didn't say which drug that was due to. But that's pretty amazing... I imagine if it works as well in lean humans as in obese mice, you could chill at 6% bf all year round feeling like a champ and eating however you want.
In fact I think I'll make this a new thread...
[/quote]
Cell Metab. 2009 Jan 7;9(1):35-51. Links
Endoplasmic reticulum stress plays a central role in development of leptin resistance.
Ozcan L, Ergin AS, Lu A, Chung J, Sarkar S, Nie D, Myers MG Jr, Ozcan U.
Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA.
Leptin has not evolved as a therapeutic modality for the treatment of obesity due to the prevalence of leptin resistance in a majority of the obese population. Nevertheless, the molecular mechanisms of leptin resistance remain poorly understood. Here, we show that increased endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) in the hypothalamus of obese mice inhibits leptin receptor signaling. The genetic imposition of reduced ER capacity in mice results in severe leptin resistance and leads to a significant augmentation of obesity on a high-fat diet. Moreover, we show that chemical chaperones, 4-phenyl butyric acid (PBA), and tauroursodeoxycholic acid (TUDCA), which have the ability to decrease ER stress, act as leptin-sensitizing agents. Taken together, our results may provide the basis for a novel treatment of obesity.
PMID: 19117545 [PubMed - indexed for MEDLINE]
Full article:
Invalid Link Removed
