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DCP 2.0

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And....we have product fitting into 2 capsules, rather than 3. This was a HUGE hurdle to pass, not only from a price point (3 caps would have increased the price by $3 a bottle) but convenience.

Should have final product very very soon.
 
And....we have product fitting into 2 capsules, rather than 3. This was a HUGE hurdle to pass, not only from a price point (3 caps would have increased the price by $3 a bottle) but convenience.

Should have final product very very soon.

Great news, man. Saw on facebook and figured that it meant it would save on cost. Stoked to give this a spin.
 
As mentioned, I had to use multiple ingredients to replace the TTA from the original formula...this is one of the main ones targeting PPAR-a.

Invalid Link Removed 2012 Jun 15;422(4):568-72. doi: 10.1016/j.bbrc.2012.05.025. Epub 2012 May 11.
[h=1]Catalposide is a natural agonistic ligand of peroxisome proliferator-activated receptor-α.[/h]Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Source[/h]Division of Food Bioscience and Technology, College of Life Sciences and Biotechnology, Korea University, Seoul 136-713, Republic of Korea.

[h=3]Abstract[/h]Peroxisome proliferator-activated receptor-alpha (PPARα) is a nuclear receptor that regulates the expression of genes related to cellular lipid uptake and oxidation. Thus, PPARα agonists may be important in the treatment of hypertriglyceridemia and hepatic steatosis. In this study, we demonstrated that catalposide is a novel natural PPARα agonist, identified from reporter gene assay-based activity screening with approximately 900 natural plant and seaweed extracts. Results of time-resolved fluorescence resonance energy transfer analyses suggested that the compound interacted directly with the ligand-binding domain of PPARα. Cultured hepatocytes stimulated with catalposide exhibited significantly reduced cellular triglyceride concentrations, by 21%, while cellular uptake of fatty acids was increased, by 70% (P<0.05). Quantitative PCR analysis revealed that the increase in cellular fatty acid uptake was due to upregulation of fatty acid transporter protein-4 (+19% vs. the control) in cells stimulated with catalposide. Additionally, expression of genes related to fatty acid oxidation and high-density lipoprotein metabolism were upregulated, while that of genes related to fatty acid synthesis were suppressed. In conclusion, catalposide is hypolipidemic by activation of PPARα via a ligand-mediated mechanism that modulates the expression of in lipid metabolism genes in hepatocytes.
Copyright © 2012 Elsevier Inc. All rights reserved.


PMID:22583896 [PubMed - indexed for MEDLINE]
 
As mentioned, I had to use multiple ingredients to replace the TTA from the original formula...this is one of the main ones targeting PPAR-a.

Invalid Link Removed 2012 Jun 15;422(4):568-72. doi: 10.1016/j.bbrc.2012.05.025. Epub 2012 May 11.
[h=1]Catalposide is a natural agonistic ligand of peroxisome proliferator-activated receptor-α.[/h]Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Source[/h]Division of Food Bioscience and Technology, College of Life Sciences and Biotechnology, Korea University, Seoul 136-713, Republic of Korea.

[h=3]Abstract[/h]Peroxisome proliferator-activated receptor-alpha (PPARα) is a nuclear receptor that regulates the expression of genes related to cellular lipid uptake and oxidation. Thus, PPARα agonists may be important in the treatment of hypertriglyceridemia and hepatic steatosis. In this study, we demonstrated that catalposide is a novel natural PPARα agonist, identified from reporter gene assay-based activity screening with approximately 900 natural plant and seaweed extracts. Results of time-resolved fluorescence resonance energy transfer analyses suggested that the compound interacted directly with the ligand-binding domain of PPARα. Cultured hepatocytes stimulated with catalposide exhibited significantly reduced cellular triglyceride concentrations, by 21%, while cellular uptake of fatty acids was increased, by 70% (P<0.05). Quantitative PCR analysis revealed that the increase in cellular fatty acid uptake was due to upregulation of fatty acid transporter protein-4 (+19% vs. the control) in cells stimulated with catalposide. Additionally, expression of genes related to fatty acid oxidation and high-density lipoprotein metabolism were upregulated, while that of genes related to fatty acid synthesis were suppressed. In conclusion, catalposide is hypolipidemic by activation of PPARα via a ligand-mediated mechanism that modulates the expression of in lipid metabolism genes in hepatocytes.
Copyright © 2012 Elsevier Inc. All rights reserved.


PMID:22583896 [PubMed - indexed for MEDLINE]

TTA going away makes me sad :( ****ers!
 
TTA going away makes me sad :( ****ers!
:::HUG:::: I know...there, there. Me too. But then again, we ended up being driven to formulate an even better product. You will not be disappointed.
 
Ha! I just remember those goo filled horse capsules from way back when. It was messy in the bottle.

You know, in spite of their guarantee, I NEVER got a refund for those. I lost over $2k from ruined product.
 
ETA 10 days.
 
YOU EXPECT ME TO WAIT 10 DAYS?!

But I'm bubbling with fat now?! SAVE ME FROM THE FAT DSADE, SAVE ME!

Srsly though, can't wait.
Sure, I can save you. Fat you say? Here, just put this apple in your mouth and come hang out in...errr, by the fire.
 
Matt, physiologically speaking, would you know any reasons why supplements or drugs that work via PPAR-a or PPAR-y would not work on a human being? I never saw much from the original DCP. I also tried what I am pretty sure was legit gw-501516 and felt absolutely nothing. Not increase in fatloss, no stamina. Makes me wonder if the new DCP might be different for people like me or if it will be a waste of money for me. Any ideas?
 
Matt, physiologically speaking, would you know any reasons why supplements or drugs that work via PPAR-a or PPAR-y would not work on a human being? I never saw much from the original DCP. I also tried what I am pretty sure was legit gw-501516 and felt absolutely nothing. Not increase in fatloss, no stamina. Makes me wonder if the new DCP might be different for people like me or if it will be a waste of money for me. Any ideas?

I wouldn't expect to 'feel' a PPAR agonist. Did you use another method of quantifying your results? I.e. did you not see changes in bodyfat or weight?
 
Matt, physiologically speaking, would you know any reasons why supplements or drugs that work via PPAR-a or PPAR-y would not work on a human being? I never saw much from the original DCP. I also tried what I am pretty sure was legit gw-501516 and felt absolutely nothing. Not increase in fatloss, no stamina. Makes me wonder if the new DCP might be different for people like me or if it will be a waste of money for me. Any ideas?
Individual expression of the PPAR isoforms varies wildly in individuals DCP 2.0 hits both alpha and delta, and includes ingredients that increase expression.
 
I wouldn't expect to 'feel' a PPAR agonist. Did you use another method of quantifying your results? I.e. did you not see changes in bodyfat or weight?

Yes, I didn't see the much loss in body fat with the original DCP. When I mentioned "feel", I was referring to GW-501516. Most report a thermogenic response, increase in fat loss and increased cardiovascular endurance. I didn't experience any of this.
 
Yes, I didn't see the much loss in body fat with the original DCP. When I mentioned "feel", I was referring to GW-501516. Most report a thermogenic response, increase in fat loss and increased cardiovascular endurance. I didn't experience any of this.

As good as it was for most not everyone responded to TTA. I'm interested to see the changes Matt makes to the formula in its absence.
 
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Sexy label!
 
Ah, DCP 2.0 has me excited...can't wait for this!
 
Invalid Link Removed 2009;16(6):888-92. Epub 2009 Dec 22.
[h=1]Activating effect of momordin, extract of bitter melon (Momordica Charantia L.), on the promoter of human PPARdelta.[/h]Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Source[/h]Department of Diabetes and Endocrinology, Saitama Medical University, Japan.

[h=3]Abstract[/h][h=4]AIM:[/h]Bitter melon (Momordica charantia L.) is a common vegetable grown in Okinawa that has also been used recently in medicine for the treatment of diseases such as diabetes, hypertension, and dyslipidemia. Among Bitter melon extracts compounds, we focused on an extract known as momordin in the present study, to examine its effect on peroxisome-proliferator activated-receptor (PPAR) delta (also called PPARdelta in rodents) expression and promoter activity of the human PPARdelta gene.
[h=4]METHODS:[/h]A human PPARdelta promoter-reporter plasmid was made as a template from a BAC CLONE (RPCI-11C) containing a -3076 bp (BglI site) +74 bp (EcoRI site) sequence. Luciferase assay of PPARdelta promoter activity was performed using HepG2 cells.
[h=4]RESULTS:[/h]10 and 25 nM Momordin significantly increased the expression of PPARdelta mRNA 1.5-fold (relative to the control). Moreover, 10 and 25 nM Momordin significantly increased PPARdelta promoter activity in a dose-dependent manner, reaching more than 1.5-fold relative to the control.
[h=4]CONCLUSION:[/h]Our present data obtained through successful cloning of the PPARdelta promoter demonstrate that PPARdelta production and activation are upregulated through PPARdelta promoter activity following momordin treatment.


PMID:20032574 [PubMed - indexed for MEDLINE]
 
The more I read about this product, the more impatient I get. I say we group up Ocean's 11 style and rob dsade of all his hard work.
 
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