Does anyone have access to the science described in this article?
Seems like the PPAR-delta receptor might be a key factor to triggering the fat burning process. Wondering if there is another way to stimulate this through whole food, or some other combination there of?
The downside for the drug look quite dramatic, but if there is a natural way to leverage this, I’m all in.
The name of the black market Drug is listed here.
It is a PPAR delta agonist.
You’ll never be able to put exercise in a bottle.
Keto increases HDL and lowers triglycerides so it probably interacts with this gene.
As far as I am concerned, the ketogenic way of eating is “triggering the fat burning process” well enough to be getting on with. Down sixty pounds in six months so far. Besides, bacon is a lot tastier than taking a pill! 
I did a bit of digging about how PPARD (PPAR delta).
PPAR delta is stimulated by dietary fatty acids and other agonists (GW501516)
How PPAR delta receptor is resulting in the burning of fat
The scientists achieved these effects by modifying a gene called PPAR-delta, a master regulator of numerous genes. Evans and his colleagues showed that by enhancing PPAR-delta’s activity, they had shifted the genetic network in muscle cells to favor burning fat over sugar as their energy source. But the effects seen in the marathon mice were caused by a genetic manipulation that was present in their bodies as their muscles were developing. Evans’s group began to wonder whether they could duplicate these effects by turning on PPAR-delta in adult mice.
@richard - I know you love ATP reading 
The scientists were intrigued by this synergistic interaction and wanted to know how exercise allowed the drug to work. One possibility was an enzyme called AMP kinase (AMPK). During exercise, cells burn ATP as their primary source of energy. In the process, they create a by-product called AMP. When cells sense the presence of AMP, they activate AMPK. Activation of AMPK creates more ATP for the cell to burn. AMPK also triggers changes that lower blood sugar, sensitize cells to insulin, enable cells to burn more fat, suppress inflammation, and otherwise influence metabolic pathways. This is one reason that exercise is so beneficial.
Evans’s team found that in addition to replenishing the cell’s energy stores, AMPK also assists PPAR-delta in activating its gene targets. “It hops onto PPAR-delta in the nucleus and turbo-charges its transcriptional activity,” Evans explained. “We think AMPK activity is the secret to allowing PPAR-delta drugs to work.”
A metabolomic study of the PPARd agonist GW501516 for enhancing running endurance in Kunming mice
https://www.nature.com/articles/srep09884
Protein May Be Linked to the Development of Colon Cancer - YouTube
people taking GW501516
http://forums.lylemcdonald.com/archive/index.php?t-23228.html
Sesamin is a naturally occurring lignan found in sesame seeds and oil. A lignan is a molecule that combines with a receptor or another entity acting as an “activator.”
Sesamin has been shown to be a potent PPAR-alpha agonist (Ide et al. 2003).
PPAR-Delta Improves Endurance by Reducing Glucose and Increasing Fat Metabolism
http://medicalfan.com/health-fitness-food/ppar-delta-improves-endurance-by-reducing-glucose-and-increasing-fat-metabolism/
http://www.cell.com/cell-metabolism/abstract/S1550-4131(17)30211-5
https://dspace.mit.edu/openaccess-disseminate/1721.1/106594
Beyaz, Semir et al. “High-Fat Diet Enhances Stemness and
Tumorigenicity of Intestinal Progenitors.” Nature 531.7592
(2016): 53–58.
As Published http://dx.doi.org/10.1038/nature17173
Abstract
Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here
we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5
+
intestinal stem-cells (ISCs) of the mammalian intestine. Mechanistically, HFD induces a robust
peroxisome proliferator-activated receptor delta (PPAR-d) signature in intestinal stem and (nonISC)
progenitor cells, and pharmacologic activation of PPAR-d recapitulates the effects of a HFD
on these cells. Like a HFD, ex vivo treatment of intestinal organoid cultures with fatty acid
constituents of the HFD enhances the self-renewal potential of these organoid bodies in a PPAR-d
dependent manner. Interestingly, HFD- and agonist-activated PPAR-d signaling endow organoidinitiating
capacity to progenitors, and enforced PPAR-d signaling permits these progenitors to
form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how dietmodulated
PPAR-d activation alters not only the function of intestinal stem and progenitor cells,
but also their capacity to initiate tumors.
Its a known fact that the fat-making process in the liver is completely controlled by PPAR delta, whereas the fat-burning process in muscle is controlled by PPAR alpha.
8 Benefits of Cardarine (GW501516) – and Risks, Side Effects
I certainly wouldn’t take any drugs that play with this system. It appears quite risky.
Hummmmm, I think I would prefer a little more fatty tissue to cancer. I already have genes that put me at risk for colon cancer, so no meds needed for that in my body.
I’m just going to keep eating lchf, fasting, and walking and doing doing strength training.
Thanks for all the great info on this topic VLC.MD. This is why I spend so much time on the forums here.
I’ve tried pioglitazone, a PPAR gamma agonist, commonly prescribed for T2DM and shown beneficial in mouse models of my muscle wasting disease, SBMA, which results in nuclear aggregations of unrecyclable misfolded androgen receptor protein that can interfere with transcription of other proteins such as the PPARs. If other PPAR agonists show promise for treating my disease and make it through the regulatory approval processes I’d want to try them too.
At current black market prices for GW501516 and related drugs iatrogenic poverty is a significant risk.
I asked for the science and you delivered. Thanks.
PS, I agree - JUST SAY NO TO PILLS, but like Keto being a focused change, I only wonder if there is a way to do an N+1 experiment and somehow naturally accelerate the internal metabolic process. Hey who knows maybe Bacon is the key.
I haven’t read all those studies yet (but will!) and will share if there are any additional insights.
Thanks again everyone. KCKO
