DCP 2.0 research - AnabolicMinds.com

DCP 2.0 research

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    DCP 2.0 research


    Hate to say it, but TTA as a viable ingredient's days are numbered. BB.com has refused to pick up any further product.

    However, I have found a way around it and we will likely phase off the TTA within the next 2 batches. For this next, however, instead of creating a new mitochondrial enhancement product right off the bat, we're going to try hard to add the Momordin to the DCP formula.

    Biochem Biophys Res Commun. 2010 Jan 15;391(3):1567-72. Epub 2009 Dec 27.
    Activation of PPARdelta up-regulates fatty acid oxidation and energy uncoupling genes of mitochondria and reduces palmitate-induced apoptosis in pancreatic beta-cells.

    Wan J, Jiang L, Lü Q, Ke L, Li X, Tong N.

    Department of Endocrinology, West China Hospital of Sichuan University, 37 Guoxue Lane, Chengdu, Sichuan 610041, China.
    Abstract

    Recent evidence indicates that decreased oxidative capacity, lipotoxicity, and mitochondrial aberrations contribute to the development of insulin resistance and type 2 diabetes. The goal of this study was to investigate the effects of peroxisome proliferator-activated receptor delta (PPARdelta) activation on lipid oxidation, mitochondrial function, and insulin secretion in pancreatic beta-cells. After HIT-T15 cells (a beta-cell line) were exposed to high concentrations of palmitate and GW501516 (GW; a selective agonist of PPARdelta), we found that administration of GW increased the expression of PPARdelta mRNA. GW-induced activation of PPARdelta up-regulated carnitine palmitoyltransferase 1 (CPT1), long-chain acyl-CoA dehydrogenase (LCAD), pyruvate dehydrogenase kinase 4 (PDK4), and uncoupling protein 2 (UCP2); alleviated mitochondrial swelling; attenuated apoptosis; and reduced basal insulin secretion induced by increased palmitate in HIT cells. These results suggest that activation of PPARdelta plays an important role in protecting pancreatic beta-cells against aberrations caused by lipotoxicity in metabolic syndrome and diabetes.
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    Mol Cell Biochem. 2010 Jun 24. [Epub ahead of print]
    Activation of PPARdelta promotes mitochondrial energy metabolism and decreases basal insulin secretion in palmitate-treated beta-cells.

    Jiang L, Wan J, Ke LQ, Lü QG, Tong NW.

    Department of Endocrinology, West China Hospital, Sichuan University, 37 Guoxue Xiang, Chengdu, Sichuan, 610041, China, jiang_li71@163.com.
    Abstract

    The peroxisome proliferator-activated receptor delta (PPARdelta) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARdelta in insulin-secreting beta-cells, however, is not well understood; we recently identified the cell-specific role of PPARdelta on mitochondrial energy metabolism and insulin secretion in lipotoxic beta-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic beta-cell line, with high concentrations of palmitate and/or the specific PPARdelta agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1alpha), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1alpha, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated beta-cells. GW501516-induced activation of PPARdelta enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic beta-cells.

    PMID: 20571903 [PubMed - as supplied by publisher]
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    Momordin study. My experimentation with high dose Bitter Melon was quite successful.

    J Atheroscler Thromb. 2009;16(6):888-92. Epub 2009 Dec 22.
    Activating effect of momordin, extract of bitter melon (Momordica Charantia L.), on the promoter of human PPARdelta.

    Sasa M, Inoue I, Shinoda Y, Takahashi S, Seo M, Komoda T, Awata T, Katayama S.

    Department of Diabetes and Endocrinology, Saitama Medical University, Japan.
    Abstract

    AIM: 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.

    METHODS: 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.

    RESULTS: 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.

    CONCLUSION: 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]
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    Havent heard the whispers.. why is TTA numbered?
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    I'm also finding some evidence for the inclusion of a Carnitine Fumerate/PLCAR blend rather than straight PLCAR. Interesting study showing Malate's (citrulline malate, for example) effects on repiratory effects and citric acid cycle flux.

    J Biol Chem. 1977 Feb 25;252(4):1309-15.
    Mitochondrial metabolism of pyruvate in bovine spermatozoa.

    Hutson SM, Van Dop C, Lardy HA.
    Abstract

    Treatment with the polyene antibiotic, filipin, renders the spermatozoan cell membrane permeable to small molecules, but not to the intracellular enzymes aldolase and lactate dehydrogenase. Pyruvate (10 mM) as the sole substrate was metabolized very slowly. L-Carnitine increased pyruvate metabolism 3- to 4-fold and allowed limited rates of oxidative phosphorylation. When spermatozoa treated with filipin were supplemented with malate, there was a rapid, almost linear rate of pyruvate metabolism which was slightly increased by L-carnitine. In the absence of malate, 20 to 30% of the pyruvate used was reduced to lactate; this increased to 57% in the presence of malate. Without malate, about 90% of the pyruvate metabolized was converted to lactate and acetate or L-acetylcarnitine. Rutamycin or rotenone increased both the rate of pyruvate use and the delta lactate/deltapyruvate ratio. Under all treatments, L-carnitine consistently reduced the percentage of pyruvate converted to lactate by about 10%; part of the pyruvate was preferentially shunted into L-acetylcarnitine rather than lactate. The mitochondrial inhibitors, rotenone or rutamycin, did not change the amount of pyruvate that was converted to metabolites other than lactate, or L-acetylcarnitine, or both. Pyruvate-supported State 3 respiration was linear only if L-carnitine, or malate, or both, were added to the incubation medium. Added malate was necessary to produce a rapid State 3 respiratory rate and was also required for significant respiratory activity in the presence of rotenone or rutamycin. From cells metabolizing [2-14C]pyruvate (1.4 mM), 14C-labeled acid-extractable metabolites were separated by ion exchange column chromatography. All of the [2-14C]pyruvate (+/-5%) used was recovered in 14C-labeled metabolites and 14CO2. In the presence of malate, citrate accumulation was significant, and was always large in comparison to flux through the citric acid cycle. Glutamate, beta-hydroxybutyrate, acetoacetate, fumarate, aspartate, and alpha-ketoglutarate did not accumulate in significant amounts. Some 14C-labeled succinate was produced but only in the presence of malate. Alkaline hydrolysis of a fraction containing carnitine esters yielded acetate and a compound tentatively identified as beta-hydroxybutyrate or lactate. As in intact cells, intramitochondrial lactate dehydrogenase competes successfully with the electron transport system for the NADH generated by pyruvate metabolism. The role of lactate and L-carnitine, and conclusions suggested by the accumulation of certain metabolites are discussed in relation to control of citric acid cycle activity.
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    PPAR delta and SIRT1: Drink your red wine!

    Endocr J. 2010;57(5):403-13. Epub 2010 Feb 17.
    PPARbeta/delta regulates the human SIRT1 gene transcription via Sp1.

    Okazaki M, Iwasaki Y, Nishiyama M, Taguchi T, Tsugita M, Nakayama S, Kambayashi M, Hashimoto K, Terada Y.

    Department of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Nankoku, Japan.
    Abstract

    NAD-dependent deacetylase SIRT1 is known to be activated by caloric restriction and is related to longevity. A natural polyphenolic compound resveratrol is also shown to increases SIRT1 activity and extends lifespan. However, the transcriptional regulation of SIRT1 gene has not completely examined in the context of metabolism. Thus, in this study, we characterized the 5' -flanking region of human SIRT1 gene. We first found that representative metabolic hormones and related factors (glucocorticoid, glucagon/cAMP, and insulin) did not show significant effect on SIRT1 gene transcription. PPARalpha and PPARgamma1 without/with their specific ligands did not have significant effect as well. In contrast, expression of PPARbeta/delta (PPARdelta markedly increased the 5' -promoter activity of SIRT1 gene, which was further amplified by the addition of GW501516, a selective PPARdelta agonist. Deletion/mutation mapping analyses failed to identify PPAR binding element but revealed the presence of canonical Sp1 binding site, which was conserved among species. The Sp1 site is functional, because Sp1 overexpresson significantly enhanced SIRT1 promoter activity, and the binding of Sp1 to the element was confirmed by EMSA and ChIP assays. Interestingly, specific Sp1 antagonist mithramycin completely abolished the PPARdelta-mediated induction of SIRT1 gene transcription. Altogether, our data suggest the predominant role of PPARdelta in the transcriptional regulation of SIRT1 gene. Furthermore, the effects of PPARdelta seem to be mediated by Sp1. We assume that, in vivo, starvation increases lipolysis-derived free fatty acid and activates PPARdelta and the resultant increase in SIRT1 expression, in addition to the activation by NAD and AMPK, facilitates the deacetylation of a variety of proteins involved in mitochondrial beta-oxidation pathway and cell survival
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    Quote Originally Posted by DAdams91982 View Post
    Havent heard the whispers.. why is TTA numbered?
    1. Not DSHEA compliant
    2. entering phase III trials (i believe) for a lipid control medication.

    Pure EPA actually looks pretty promising, and I can get an algae derived version...just nothing at the same small dose as TTA unfortunately, without some molecular modifications, which would then again DQ it from DSHEA.
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    I like the sounds of this so far. The ingredients above sem like solid additions. You think this will be here for winter recomps?
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    Quote Originally Posted by phantom View Post
    I like the sounds of this so far. The ingredients above sem like solid additions. You think this will be here for winter recomps?
    I'm waiting for final price of the Momordin and quick sample for production, but we're hoping to have it by Thanksgiving.
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    That would be even better-holiday binging isn't the same without DCP lol the plcar/fumerate combo sounds pretty solid as well-and cant go wrong with good qualtiy EPA
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    Can't wait...DCP was one of my favorite products when it was around so I look forward to a newer version!
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    Lipids. 2009 Dec;44(12):1073-9. Epub 2009 Oct 27.

    n-3 PUFA as regulators of cardiac gene transcription: a new link between PPAR activation and fatty acid composition.
    Di Nunzio M, Danesi F, Bordoni A.

    Department of Biochemistry G. Moruzzi, Alma Mater Studiorum, University of Bologna, 40126, Bologna (BO), Italy.

    Abstract
    The fatty acids regulate gene expression directly binding to nuclear receptors or affecting the protein content of transcription factors. In this work, supplementing primary cultures of neonatal rat cardiomyocytes with 60 microM EPA or DHA, we demonstrated by an ELISA assay an increased PPAR beta/delta binding to DNA. n-3 PUFA supplementation deeply changed the acyl composition of both cytosolic and nuclear fractions. The high content of total fatty acids, particularly EPA and DHA, and its increase following supplementation suggested a selective accumulation of n-3 PUFAs in the nucleus, supporting the direct interaction of n-3 PUFA with PPAR. The activity of acyl-CoA thioesterase (ACOT), catalyzing the reaction leading to NEFA from acyl-CoA, increased in n-3 PUFA supplemented cells. The NEFA/acyl-CoA ratio is an important regulator of the fatty acid transport to the nucleus and consequent modulation of gene transcription, and although ACOT activity is not the only parameter of this ratio, it is important for the control of the NEFA pool composition. Our data further clarify what happens in cardiomyocytes following n-3 PUFA supplementation, linking the modification of acyl composition to ACOT activity and PPAR activation.
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    What about adding GPA and rhodiola?
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    Quote Originally Posted by Autobody View Post
    What about adding GPA and rhodiola?
    GPA has a limited application, and it's not long-term supplementation.

    Can you clarify a reasoning behind Rhodiola, specifically as it relates to mitochondrial or peroxisomal activity?
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    I've never noticed much from rhodolia. I find it makes me tired more than anything.
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    A little Rhodiola info from Life Extension:

    One of the best herbs for enhancing mitochondrial energy production is Rhodiola rosea. Also known as golden root or Arctic root, rhodiola has been used in traditional medicine for centuries. It has been studied extensively by Russian scientists, who have dubbed it an adaptogen. This term refers to the herb’s ability to increase resistance to numerous chemical, physical, and biological stressors, including strenuous exertion, mental strain, and toxic chemicals.42

    A recent study in rats that were trained to exhaustion found that rhodiola significantly boosted the synthesis and resynthesis of ATP in the mitochondria, which enabled the rats to swim for 24% longer.43 Rhodiola also reduces fatigue under stressful conditions and exerts an anti-inflammatory effect.44,45 Richard Brown, MD, assistant professor of clinical psychiatry at Columbia University and author of The Rhodiola Revolution, recommends it as an energy booster and treatment for depression, chronic fatigue, and anxiety.46

    In a randomized, double-blind, placebo-controlled trial with medical students, Russian researchers showed that rhodiola extract improves the capacity to perform mentally demanding tasks under conditions of extreme stress and fatigue.44 A similarly controlled trial conducted on students during a stressful examination period found that objective and subjective measures of physical and mental performance were significantly superior among subjects who took rhodiola extract compared to placebo.47 It is believed that rhodiola’s beneficial properties stem in part from its ability to influence the activities and levels of brain chemicals such as serotonin and norepinephrine, as well as natural “feel good” opioids such as beta-endorphins.48

    42. Anon. Rhodiola rosea. Monograph. Altern Med Rev. 2002 Oct;7(5):421-3.

    43. Abidov M, Crendal F, Grachev S, Seifulla R, Ziegenfuss T. Effect of extracts from Rhodiola rosea and Rhodiola crenulata (Crassulaceae) roots on ATP content in mitochondria of skeletal muscles. Bull Exp Biol Med. 2003 Dec;136(6):585-7.

    44. Shevtsov VA, Zholus BI, Shervarly VI, et al. A randomized trial of two different doses of a SHR-5 Rhodiola rosea extract versus placebo and control of capacity for mental work. Phytomedicine. 2003 Mar;10(2-3):95-105.

    45. Abidov M, Grachev S, Seifulla RD, Ziegenfuss TN. Extract of rhodiola rosea radix reduces the level of C-reactive protein and creatinine kinase in the Blood. Bull Exp Biol Med. 2004 Jul;138(1):63-4.
    46. Brown RP, Gerbarg PL, Graham B. The Rhodiola Revolution: Transform Your Health with the Herbal Breakthrough of the 21st Century. Emmaus, PA: Rodale Books; 2004.

    47. Spasov AA, Wikman GK, Mandrikov VB, Mironova IA, Neumoin VV. A double-blind, placebo-controlled pilot study of the stimulating and adaptogenic effect of Rhodiola rosea SHR-5 extract on the fatigue of students caused by stress during an examination period with a repeated low-dose regimen. Phytomedicine. 2000 Apr;7(2):85-9.

    48. Kelly GS. Rhodiola rosea: a possible plant adaptogen. Altern Med Rev. 2001 Jun;6(3):293-302
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    hmmmm wounder if we could run some of the old dcp stacked with some of the new,

    4 caps old, 4 caps new should be a nice stack
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    The old DCP was amazing stuff, I have great faith the new version will be a solid step in enhancement progression.
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    Old DCP was one of my favorites, wish I had some...I am a huge fan of mitochondrial enhancement supplementation.

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    Why not use sesamin?
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    DCP is hands down the best non-stim fatburner I've ever used. It stacks so well with many different products. It's sad to hear that the TTA will be going away, but I have nothing but faith in the new version you're working on, Matt.

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    Quote Originally Posted by TripDog View Post
    The old DCP was amazing stuff, I have great faith the new version will be a solid step in enhancement progression.
    I don't come here very often but weren't you with GetDiesel a while ago?

    When did they leave the board?

    Quote Originally Posted by acshadow View Post
    Why not use sesamin?
    Sesamin has some drawbacks in my opinion. Maybe there's a fine line between effective and counterproductive and I'm not sure what that is...
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    I just posted this in the supplement forum as well. Have you seen this stuff before Matt?

    LOWAT™ is a patent-pending weight management ingredient consisting of Piper betle leaf and Dolichos biflorus seed extracts that has been clinically shown to promote weight loss. These natural extracts uniquely combine to target fat. Clinical research has shown that LOWAT™ significantly increases serum adiponectin concentration, indicating a possible reduction in fat stores. Adiponectin, a hormone produced and secreted by fat cells, regulates the breakdown of fat. Preliminary research suggests that LOWAT™ inhibits adipogenesis (generation and accumulation of fat in the fat cells) and increases lipolysis (breakdown of stored fat) in mature fat cells. LOWAT™ has been shown in randomized, double-blind, placebo-controlled research to significantly reduce body weight 2.4x better than placebo after eight weeks. While weight loss was already evident two weeks into the study, significant weight loss of around 9 lbs was seen at week eight.
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    Quote Originally Posted by acshadow View Post
    Why not use sesamin?
    Sesamin would be a good add-on, however...

    The original source that I engaged to make the incredible SesaThin raised the price and minimums significantly, making it not a good value for the effectiveness.

    Sesamin is primarily a PPAR-Alpha agonist, whereas the DCP product is dependent upon PPAR-Delta activation - highly rare in naturally ocurring compounds.
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    Quote Originally Posted by jdrannin1 View Post
    I don't come here very often but weren't you with GetDiesel a while ago?

    When did they leave the board?



    Sesamin has some drawbacks in my opinion. Maybe there's a fine line between effective and counterproductive and I'm not sure what that is...
    what drawbacks are u referring to?
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    Quote Originally Posted by dsade View Post
    Sesamin would be a good add-on, however...

    The original source that I engaged to make the incredible SesaThin raised the price and minimums significantly, making it not a good value for the effectiveness.

    Sesamin is primarily a PPAR-Alpha agonist, whereas the DCP product is dependent upon PPAR-Delta activation - highly rare in naturally ocurring compounds.
    The only one that comes to mind is GW1516. I seen you have references of it in your leading posts. Did you find a natural source for a delta agonist?
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    bump for Momordin
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    ?? Im lost LOL



    Are they adding this?

    Quote Originally Posted by MAxximal View Post
    bump for Momordin
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    Quote Originally Posted by dsade View Post
    Momordin study. My experimentation with high dose Bitter Melon was quite successful.

    J Atheroscler Thromb. 2009;16(6):888-92. Epub 2009 Dec 22.
    Activating effect of momordin, extract of bitter melon (Momordica Charantia L.), on the promoter of human PPARdelta.

    Sasa M, Inoue I, Shinoda Y, Takahashi S, Seo M, Komoda T, Awata T, Katayama S.

    Department of Diabetes and Endocrinology, Saitama Medical University, Japan.
    Abstract

    AIM: 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.

    METHODS: 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.

    RESULTS: 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.

    CONCLUSION: 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]
    How do you think the Momordin stacks up agains TTA, If I am understanding correctly the only drawback is that the dose is larger, so there will be larger/more caps. I am using DCP for the first time right now and it is working beautifully. Hate that there has to be changes.
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    Def sounds interesting.. tta is some good stuff, so it will be very hard to beat IMO.

    Mike
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    Why was the TTA removed?
    A-Minds HYPE-SLAYER! All posts & feedback are guaranteed to be unsolicited and legit
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    Quote Originally Posted by Whacked View Post
    Why was the TTA removed?
    Big Pharma wants it and are doing trials on it currently. So once they make it a prescription bye bye tta for us.
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    Quote Originally Posted by truthornothin View Post
    How do you think the Momordin stacks up agains TTA, If I am understanding correctly the only drawback is that the dose is larger, so there will be larger/more caps. I am using DCP for the first time right now and it is working beautifully. Hate that there has to be changes.
    Momordin is not there as a TTA replacement. Momordin increases expression of the PPAR-delta receptor (a very important form expressed in skeletal muscle.) TTA is an agonist of the receptor.

    Momordin will be working to increase effectiveness of the TTA replacement.
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    So what's the TTA replacement?

    Quote Originally Posted by dsade View Post
    Momordin is not there as a TTA replacement. Momordin increases expression of the PPAR-delta receptor (a very important form expressed in skeletal muscle.) TTA is an agonist of the receptor.

    Momordin will be working to increase effectiveness of the TTA replacement
    .
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    Momordica Charantia [30% Charantin]..............?
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    Quote Originally Posted by Whacked View Post
    So what's the TTA replacement?
    Given the nature of the copycats in this industry, there is NO way I am releasing any more details about the formula until we are ready for release.
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    Quote Originally Posted by ssbackwards View Post
    So....milk does a body good??
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    Ahhh gotcha - totally understandable

    Quote Originally Posted by dsade View Post
    Given the nature of the copycats in this industry, there is NO way I am releasing any more details about the formula until we are ready for release.
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    As much as I'll miss DCP, I'm excited for DCP 2.0!
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