I asked a friend who is studying biochem to become a doctor how they think SLU works. This is a summary of their response:
It probably acts through the Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). It's a protein that in humans is encoded by the PPARGC1A gene.
PGC-1α is the master regulator of mitochondria biogenesis (the increasing of mitochondria count in the body). PGC-1α is also the primary regulator of liver gluconeogensis, inducing increased gene expression for gluconeogenesis. AKA you process carbs better.
PPARGC1A has been shown to interact with:
- Estrogen-related receptor alpha (ERRα), estrogen-related receptor beta (ERR-β), estrogen-related receptor gamma (ERR-γ).
Which SLU has shown tendencies to interactive with ERR-alpha
ERRα regulates genes involved in mitochondrial biogenesis, gluconeogenesis, oxidative phosphorylation, fatty acid metabolism, and brown adipose tissue thermogenesis.
The following is now my theory, based on this info, as to why SLU might work for some, but not others.
1. Amount of brown adipose tissue. There are two types of fat, brown fat, and white fat. Brown fat allows easy access to energy from fat stores, white fat does not. Brown fat % decreases as one ages. There are methods to brown fat, like taking beta-3 agonists like mirabergon. Some people, i.e younger folks, might see better results from SLU because of this. If you're older, look into mirabergon to brown a % of your white fat.
2. Insulin Sensitivy. If you are already insulin sensitive, or perhaps use SLU when fasted, taking it to upregulate gluconegensis might put you in a state of ketosis / using fat for energy. If your insulin sensitivity is poor (i.e you are insulin resistant), it might just lower you to a still bad number. Some might not see large benefits as even with SLU, they might still have diabetitc levels of fasting insulin.
3. I discussed this one eariler, density of ERR Alpha cells. ERRα has wide tissue distribution but it is most highly expressed in tissues that preferentially use fatty acids as energy sources such as kidney, heart, brown adipose tissue, cerebellum, intestine, and muscles. Thus more muscle mass, more brown adipose tissue, and larger organs (perhaps from excessive HGH use.... speaking from experience) might get better results than others as they have more ERR Alpha Cells.
The biochemist said he'll look into it more after his mid terms. I'll update my thoughts / theories as I get more info.
As for why I think the studies used injectable, again all conjecture on my behalf, I'll share my current thoughts I pondered while not paying attention to a meeting I was in.
Solubility. Drugs that have good bioavailability are soluble in aqueous solutions (aka water, stomach acid). Speaking from experience SLU has absolutely dog shit solubility in aqueous solutions. Literally adding 0.1 mls of saline out of 1 ml to the freeze dried SLU brought it out of solution. A saving grace would be how soluble SLU is in acid. Since I am familiar with Hydrocholric Acid, which is a fairly strong acid of PH 1.6 (lower PH = stronger acid), seems like a good place to start.
"SLU-PP-332 is not soluble in hydrochloric acid; it is primarily soluble in DMSO (dimethyl sulfoxide) due to its polar nature, and adding hydrochloric acid would likely cause precipitation of the compound as it is not designed to dissolve in acidic environments"
Due to these two reasons, I highly doubt SLU has a very high oral availability if just ingested in a cap. In a solution on the other hand, that might change things. Something to look into another day.
