no, im planning a PPAR-agonist, natrural testosterone booster, T2 and ursolic acid
nothing suppresive to my testosterone
T2 is useless and a waste of your money
Ursolic acid is a PPAR-α agonist that regulates hepatic lipid metabolism.
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In this study, we confirmed that ursolic acid, a plant triterpenoid, activates peroxisome proliferator-activated receptor (PPAR)-α in vitro. Surface plasmon resonance and time-resolved fluorescence resonance energy transfer analyses do not show direct binding of ursolic acid to the ligand-binding domain of PPAR-α; however, ursolic acid enhances the binding of PPAR-α to the peroxisome proliferator response element in PPAR-α-responsive genes, alters the expression of key genes in lipid metabolism, significantly reducing intracellular triglyceride and cholesterol concentrations in hepatocytes. Thus, ursolic acid is a PPAR-α agonist that regulates the expression of lipid metabolism genes, but it is not a direct ligand of PPAR-α.
Tetradecylthioacetic Acid (TTA)
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TetradecylThioacetic Acid (TTA), a non beta-oxidizable fatty acid analog, has been shown to activate all three of the PPAR receptors in rats, in the ranking order of Alpha > Beta/Delta > Gamma (Madsen et al. 2002).
TTA has been shown to increase insulin sensitivity by increasing hepatic fat oxidation and ketogenesis while draining fatty acids from the blood and extrahepatic tissues. This drainage of fatty acids by the liver increases the ability of adipocytes and skeletal muscle in uptake glucose (Grav et al. 2003).
TTA has been shown to cause mitochondrial and peroxisomal proliferation in rats (Kryvi et al. 1990), leading to increased beta-oxidation of fatty acids in the liver, along with increasing uncoupling protein-2 (UCP-2) expression (Grav et al. 2003). UCP-2, and UCP-3, is involved in preventing the accumulation of oxygen-specific free radicals and in regulating lipogenesis and ketogenesis.
UCP-2 is found throughout the body (Grav et al. 2003). These three adaptations, increased mitochondria, peroxisomes, and UCP-2 concentrations, all aid in increasing insulin sensitivity and reducing adiposity.
Oleoylethanolamide (OEA)
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Oleoylethanolamide (OEA) is an endogenous lipid being investigated as a potential anti-obesity drug. OEA is synthesized in the intestines. Its synthesis is increased with food intake and decreased with fasting.
What Does Endogenous Mean?
Endogenous refers to something which originates internally, or is synthesized inside the body, tissues, and/or cells.
OEA has been shown to have anorexic properties, meaning it decreases food intake. A study done on rats showed that OEA's ability to decrease appetite did not change plasma levels of various intestinal hormones involved in satiety, such as ghrelin and CCK, showing OEA works independently of these hormones (Proulx et al. 2005).
OEA is also an activator of the PPAR receptor (Fu et al. 2005). Activation of PPARalpha by OEA will cause an increase in fat oxidation along with a decrease in fat storage, as described in the above sections. OEA's ability to decrease appetite and regulate body weight is accomplished by the activation of PPARalpha (Fu et al. 2003).