In support of Patrick's product; I would like to show what part of the ursolic acid research I like. I would hope for some contributing chatter thereafter.
First, we'll look at some PPAR work (for which I have been meaning to do a separate thread for; time is always an issue unfortunately)...
Bioorg Med Chem Lett. 2011 Oct 1;21(19):5876-80. Epub 2011 Aug 3.
Ursolic acid is a PPAR-α agonist that regulates hepatic lipid metabolism.
Jia Y, Bhuiyan MJ, Jun HJ, Lee JH, Hoang MH, Lee HJ, Kim N, Lee D, Hwang KY, Hwang BY, Choi DW, Lee SJ.
Source
Department of Biotechnology, Graduate School of Biotechnology, Korea University, Seoul 136-713, Republic of Korea.
Abstract
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.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID:
21855333
[PubMed - in process]
PPAR-alpha activation increases the expression of lipoprotein lipase and apolipoprotein A-V (apoA-V) while simultaneously decreasing expression of apoC-III in the liver, which decreases VLDL particles and lowering plasma triglycerides in chylomicrons. These changes liberate fatty acids, allowing them to either be oxidized or stored. This suggests that use of a PPAR-alpha agonist may be beneficial in aiding fat loss. In addition to the change in plasma fatty acid levels, hepatic apoA-I andapoA-II are increased by PPAR-alpha activation, which improves cholesterol levels by increasing HDL levels.
Now, many may not be familiar with the benefits of elevated HDL cholesterol - however, in my world, HDL trumps all other cholesterol numbers. In cycling bodybuilders...it is the first number to "go bad (lowers)." There are many that harbor an isolated low HDL syndrome and understand that while decreasing LDL holds superiority in clinical trials because we have many drugs that could lower it, the impact in my estimation is simply the anti-inflammatory nature of statins providing the benefit as opposed to true lowering of LDL - and lowering LDL actually constitutes a MINORITY of coronary heart disease in the full spectrum.
I think in the world of bodybuilding ursolic acid may provide an additional agent of natural HDL increments; alongside niacin. Coupling the two together are probably a good ancillary protocol for anabolic-androgenic-induced dyslipidemia (AAID); although currently I use HMB + Pantothene + Niacin for reasons that are well beyond the scope of this post.
D_
First, we'll look at some PPAR work (for which I have been meaning to do a separate thread for; time is always an issue unfortunately)...
Bioorg Med Chem Lett. 2011 Oct 1;21(19):5876-80. Epub 2011 Aug 3.
Ursolic acid is a PPAR-α agonist that regulates hepatic lipid metabolism.
Jia Y, Bhuiyan MJ, Jun HJ, Lee JH, Hoang MH, Lee HJ, Kim N, Lee D, Hwang KY, Hwang BY, Choi DW, Lee SJ.
Source
Department of Biotechnology, Graduate School of Biotechnology, Korea University, Seoul 136-713, Republic of Korea.
Abstract
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.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID:
21855333
[PubMed - in process]
PPAR-alpha activation increases the expression of lipoprotein lipase and apolipoprotein A-V (apoA-V) while simultaneously decreasing expression of apoC-III in the liver, which decreases VLDL particles and lowering plasma triglycerides in chylomicrons. These changes liberate fatty acids, allowing them to either be oxidized or stored. This suggests that use of a PPAR-alpha agonist may be beneficial in aiding fat loss. In addition to the change in plasma fatty acid levels, hepatic apoA-I andapoA-II are increased by PPAR-alpha activation, which improves cholesterol levels by increasing HDL levels.
Now, many may not be familiar with the benefits of elevated HDL cholesterol - however, in my world, HDL trumps all other cholesterol numbers. In cycling bodybuilders...it is the first number to "go bad (lowers)." There are many that harbor an isolated low HDL syndrome and understand that while decreasing LDL holds superiority in clinical trials because we have many drugs that could lower it, the impact in my estimation is simply the anti-inflammatory nature of statins providing the benefit as opposed to true lowering of LDL - and lowering LDL actually constitutes a MINORITY of coronary heart disease in the full spectrum.
I think in the world of bodybuilding ursolic acid may provide an additional agent of natural HDL increments; alongside niacin. Coupling the two together are probably a good ancillary protocol for anabolic-androgenic-induced dyslipidemia (AAID); although currently I use HMB + Pantothene + Niacin for reasons that are well beyond the scope of this post.
D_