GW-501516 (Cardarine)

[bigbumpkin2003]

I'm about to partake in this at 20 per day for 30 days.

If people want a log I'd be happy to run one. Helps keep me accountable too

 

[johnjuanb1]

I'm about to partake in this at 20 per day for 30 days.

If people want a log I'd be happy to run one. Helps keep me accountable too

Yes, please run a log but don't title it log or it gets moved to the logs section which is dead. Just title it GW

 

[bigbumpkin2003]

Yes, please run a log but don't title it log or it gets moved to the logs section which is dead. Just title it GW

Ok. Thanks for tip. My avatar is really old lol. But talkatap still lets me post pics. So I'll get a good set of starting ones..front back side legs and scale weight. Then do same and end of run in same room so lighting etc is all same and doesn't skew anything. I was very skeptical of peptides and mk-677 but every thing I have run has blown my socks off!!

 

[bigbumpkin2003]

I've received one of my two bottles! Hmmmm. Contacted company waiting to hear back

 

[Tawab]

It's best taken 30-45 minutes before a workout. You can dose it once a day or split dose it.

Why would you even bother 30-45 minutes before? it is active for over 23 hours so it doesn't matter if it's 10 minutes or 10 hours before...

 

[DORIAN*]

I'm about to partake in this at 20 per day for 30 days.

If people want a log I'd be happy to run one. Helps keep me accountable too

I should be doing the same too. Gonna order some in a few days to try out. At worst I hope it helps with my cardio as I am on tren as the moment.

 

[johnjuanb1]

2015 GW-501516 pubmed study

A metabolic study of the PPARδ agonist GW501516 for enhancing running endurance in Kunming mice.
Chen W, et al. Sci Rep. 2015.

Abstract

Exercise can increase peroxisome proliferator-activated receptor-δ (PPARδ) expression in skeletal muscle. PPARδ regulates muscle metabolism and reprograms muscle fibre types to enhance running endurance. This study utilized metabolomic profiling to examine the effects of GW501516, a PPARδ agonist, on running endurance in mice. While training alone increased the exhaustive running performance, GW501516 treatment enhanced running endurance and the proportion of succinate dehydrogenase (SDH)-positive muscle fibres in both trained and untrained mice. Furthermore, increased levels of intermediate metabolites and key enzymes in fatty acid oxidation pathways were observed following training and/or treatment. Training alone increased serum inositol, glucogenic amino acids, and branch chain amino acids. However, GW501516 increased serum galactose and β-hydroxybutyrate, independent of training. Additionally, GW501516 alone raised serum unsaturated fatty acid levels, especially polyunsaturated fatty acids, but levels increased even more when combined with training. These findings suggest that mechanisms behind enhanced running capacity are not identical for GW501516 and training. Training increases energy availability by promoting catabolism of proteins, and gluconeogenesis, whereas GW501516 enhances specific consumption of fatty acids and reducing glucose utilization.

 

[dragonfire101]

BUMP any cardoivascular studies ?

 

[johnjuanb1]

BUMP any cardoivascular studies ?

PPARβ/δ activation blocks lipid-induced inflammatory pathways in mouse heart and human cardiac cells.
Alvarez-Guardia D, et al. Biochim Biophys Acta. 2011.

Abstract

Owing to its high fat content, the classical Western diet has a range of adverse effects on the heart, including enhanced inflammation, hypertrophy, and contractile dysfunction. Proinflammatory factors secreted by cardiac cells, which are under the transcriptional control of nuclear factor-κB (NF-κB), may contribute to heart failure and dilated cardiomyopathy. The underlying mechanisms are complex, since they are linked to systemic metabolic abnormalities and changes in cardiomyocyte phenotype. Peroxisome proliferator-activated receptors (PPARs) are transcription factors that regulate metabolism and are capable of limiting myocardial inflammation and hypertrophy via inhibition of NF-κB. Since PPARβ/δ is the most prevalent PPAR isoform in the heart, we analyzed the effects of the PPARβ/δ agonist GW501516 on inflammatory parameters. A high-fat diet induced the expression of tumor necrosis factor-α, monocyte chemoattractant protein-1, and interleukin-6, and enhanced the activity of NF-κB in the heart of mice. GW501516 abrogated this enhanced proinflammatory profile. Similar results were obtained when human cardiac AC16 cells exposed to palmitate were coincubated with GW501516. PPARβ/δ activation by GW501516 enhanced the physical interaction between PPARβ/δ and p65, which suggests that this mechanism may also interfere NF-κB transactivation capacity in the heart. GW501516-induced PPARβ/δ activation can attenuate the inflammatory response induced in human cardiac AC16 cells exposed to the saturated fatty acid palmitate and in mice fed a high-fat diet. This is relevant, especially taking into account that PPARβ/δ has been postulated as a potential target in the treatment of obesity and the insulin resistance state.

 

[johnjuanb1]

This study is exactly what I was looking for.
I'm searching for all wound healing drugs to add to my Arsenal.

PPARdelta promotes wound healing by up-regulating TGF-beta1-dependent or -independent expression of extracellular matrix proteins.
Ham SA, et al. J Cell Mol Med. 2010.

Abstract

Although the peroxisome proliferator-activated receptor (PPAR) delta has been implicated in the wound healing process, its exact role and mechanism of action have not been fully elucidated. Our previous findings showed that PPARdelta induces the expression of the transforming growth factor (TGF)-beta1, which has been implicated in the deposit of extracellular matrix proteins. Here, we demonstrate that administration of GW501516, a specific PPARdelta ligand, significantly promoted wound closure in the experimental mouse and had a profound effect on the expression of collagen types I and III, alpha-smooth muscle actin, pSmad3 and TGF-beta1, which play a pivotal role in wound healing processes. Activation of PPARdelta increased migration of human epidermal keratinocytes and dermal fibroblasts in in vitro scrape-wounding assays. Addition of a specific ALK5 receptor inhibitor SB431542 significantly suppressed GW501516-induced migration of human keratinocytes and fibroblasts. In these cells, activated PPARdelta also induced the expression of collagen types I and III and fibronectin in a TGF-beta1-dependent or -independent manner. The effect of PPARdelta on the expression of type III collagen was dually regulated by the direct binding of PPARdelta and Smad3 to a direct repeat-1 site and a Smad-binding element, respectively, of the type III gene promoter. Taken together, these results demonstrated that PPARdelta plays an important role in skin wound healing in vivo and that it functions by accelerating extracellular matrix-mediated cellular interactions in a process mediated by the TGF-beta1/Smad3 signaling-dependent or - independent pathway.

PMID 19538467 [PubMed - indexed for MEDLINE] PMCID PMC3829036

 

[jrock00123]

This study is exactly what I was looking for.
I'm searching for all wound healing drugs to add to my Arsenal.

Is there anything this drugs doesn't do? Amazing.

At 5mg per day for the last two weeks. Bumping to 10mg on Tues & Thr so I can get 5mg prior to morning HIIT and another 5mg before afternoon training.

Not sure how much it is affecting overall endurance, but I feel it is making a difference keeping me fairly lean while adding scale weight.

 

[dragonfire101]

This study is exactly what I was looking for.
I'm searching for all wound healing drugs to add to my Arsenal.

So what’s that look like right now?

I’m looking for the same with the addition of any heart benefits.

So which you think tb500 and bpc 157 would have better heart benefits and or healing?

 

[johnjuanb1]

So what’s that look like right now?

I’m looking for the same with the addition of any heart benefits.

So which you think tb500 and bpc 157 would have better heart benefits and or healing?

I'm picking up my GW-501516 after I eat and shower. I'm adding it to my
TB-500 and BPC157 hoping it will increase the rate of healing in all my injuries I incurred from insulin resistance. Yesterday was the best my injuries ( left and right rotator cuff, left rear delt, left lat insert, left pec insert) have felt in a couple months. Metformin is working real well to fix the insulin resistance. I know this GE study wasn't geared towards skeletal muscle healing, but if it speeds up the rate of healing in general then it should help.

 

[johnjuanb1]

I started my GW501516 last night, 5mg twice a day. Nothing to report yet.

 

[johnjuanb1]

Metabolic syndrome is basically "Palumboism," right. The body is unable to provide nutrients to the muscles; primarily the appendages like arms and legs, so they deteriorate. GW-501516 will help fight this disorder.

Peroxisome proliferator-activated receptor (PPAR) beta/delta: a new potential therapeutic target for the treatment of metabolic syndrome.
Review article
Coll T, et al. Curr Mol Pharmacol. 2009.

Abstract

Metabolic syndrome is defined as the clustering of multiple metabolic abnormalities, including abdominal obesity, dyslipidemia (high serum triglycerides and low serum HDL-cholesterol levels), glucose intolerance and hypertension. The pathophysiology underlying metabolic syndrome involves a complex interaction of crucial factors, but two of these, insulin resistance and obesity (especially visceral obesity), play a major role. The nuclear receptors Peroxisome Proliferator-Activated Receptors (PPAR)alpha and PPARgamma are therapeutic targets for hypertriglyceridemia and insulin resistance, respectively. Evidence is now emerging that the PPARbeta/delta; isotype is a potential pharmacological target for the treatment of disorders associated with metabolic syndrome. PPARbeta/delta; activation increases lipid catabolism in skeletal muscle, heart and adipose tissue and improves the serum lipid profile and insulin sensitivity in several animal models. In addition, PPARbeta/delta; ligands prevent weight gain and suppress macrophage-derived inflammation. These data are promising and indicate that PPARbeta/delta; ligands may become a therapeutic option for the treatment of metabolic syndrome. However, clinical trials in humans assessing the efficacy and safety of these drugs should confirm these promising perspectives in the treatment of the metabolic syndrome.

 

[Smack]

I started my GW501516 last night, 5mg twice a day. Nothing to report yet.

What about now?

 

[johnjuanb1]

What about now?

My carbs are so low I'm drained. But I look so much leaner from dropping HGH and mk677. All the water retention is leaving. I don't feel endurance but I know I need a refeed. This always happens after a week on my diet.

 

[j2048b]

Metabolic syndrome is basically "Palumboism," right. The body is unable to provide nutrients to the muscles; primarily the appendages like arms and legs, so they deteriorate. GW-501516 will help fight this disorder.



Peroxisome proliferator-activated receptor (PPAR) beta/delta: a new potential therapeutic target for the treatment of metabolic syndrome.

Review article

Coll T, et al. Curr Mol Pharmacol. 2009.



Abstract



Metabolic syndrome is defined as the clustering of multiple metabolic abnormalities, including abdominal obesity, dyslipidemia (high serum triglycerides and low serum HDL-cholesterol levels), glucose intolerance and hypertension. The pathophysiology underlying metabolic syndrome involves a complex interaction of crucial factors, but two of these, insulin resistance and obesity (especially visceral obesity), play a major role. The nuclear receptors Peroxisome Proliferator-Activated Receptors (PPAR)alpha and PPARgamma are therapeutic targets for hypertriglyceridemia and insulin resistance, respectively. Evidence is now emerging that the PPARbeta/delta; isotype is a potential pharmacological target for the treatment of disorders associated with metabolic syndrome. PPARbeta/delta; activation increases lipid catabolism in skeletal muscle, heart and adipose tissue and improves the serum lipid profile and insulin sensitivity in several animal models. In addition, PPARbeta/delta; ligands prevent weight gain and suppress macrophage-derived inflammation. These data are promising and indicate that PPARbeta/delta; ligands may become a therapeutic option for the treatment of metabolic syndrome. However, clinical trials in humans assessing the efficacy and safety of these drugs should confirm these promising perspectives in the treatment of the metabolic syndrome.

This interests me very much because when i was younger i wasnt able to even make my legs grow! Arms a bit, but nothing according to the way i lifted etc..... I should have grown more but have not been able to..... Soooo if this proves to be correct, my arms and legs should grow to bigger sizes FINALLY! And hopefully everything will look as it should.... Hate having peg legs and a huge upper back and crap like that.....

 

[jrock00123]

Metabolic syndrome is basically "Palumboism," right. The body is unable to provide nutrients to the muscles; primarily the appendages like arms and legs, so they deteriorate. GW-501516 will help fight this disorder.

Peroxisome proliferator-activated receptor (PPAR) beta/delta: a new potential therapeutic target for the treatment of metabolic syndrome.
Review article
Coll T, et al. Curr Mol Pharmacol. 2009.

Abstract

Metabolic syndrome is defined as the clustering of multiple metabolic abnormalities, including abdominal obesity, dyslipidemia (high serum triglycerides and low serum HDL-cholesterol levels), glucose intolerance and hypertension. The pathophysiology underlying metabolic syndrome involves a complex interaction of crucial factors, but two of these, insulin resistance and obesity (especially visceral obesity), play a major role. The nuclear receptors Peroxisome Proliferator-Activated Receptors (PPAR)alpha and PPARgamma are therapeutic targets for hypertriglyceridemia and insulin resistance, respectively. Evidence is now emerging that the PPARbeta/delta; isotype is a potential pharmacological target for the treatment of disorders associated with metabolic syndrome. PPARbeta/delta; activation increases lipid catabolism in skeletal muscle, heart and adipose tissue and improves the serum lipid profile and insulin sensitivity in several animal models. In addition, PPARbeta/delta; ligands prevent weight gain and suppress macrophage-derived inflammation. These data are promising and indicate that PPARbeta/delta; ligands may become a therapeutic option for the treatment of metabolic syndrome. However, clinical trials in humans assessing the efficacy and safety of these drugs should confirm these promising perspectives in the treatment of the metabolic syndrome.

Metabolic syndrome is basically a set of related symptoms. The underlying cause seems to be insulin resistance. I wouldn't necessarily equate this with "Palumboism".

 

[johnjuanb1]

Metabolic syndrome is basically a set of related symptoms. The underlying cause seems to be insulin resistance. I wouldn't necessarily equate this with "Palumboism".

I was wondering if severe insulin resistance leads to Palumboism?