Bulk Berberine
- Thread starter dsade
- Start date
johnfaceman
Active member
Damn D, how am I suppose to order the whole stock if you go advertising it. Keep us updated brotha!:cheers:
johnfaceman
Active member
I know it is in Alri Lean Dreams.
johnfaceman
Active member
Jayhawkk said:Berberine seems to be the 'in' topic at the moment
Yea just saw what you are talking about :head:
WannaBeHulk
rollin' on dubs!
i think its dsades capped concoction that nutra will be carrying standing for Damage Control Protocol. very good idea IMORodja said:
WhatsaRoid?
Board Sponsor
Lets be real man, how does that bulk Berberine compare to AP? I jus want the bulk Berberine to add to everything else I have I don't need the stack. how soon will Berberine be up for purchase?
Last edited:
WannaBeHulk
rollin' on dubs!
very true but i think it will be marketed to use when the diet is subpar or slacking... i.e. the holiday season, on vacation, or the infamous cheats. i would like it for contest prep myselfRodja said:
prld2gr8ns
Idiot Savant
Similiar in that it's a percentage of the whole, have no idea how ithwould be dosed though, but my guess would be in much larger quanities then AP.I-Vtec said:is this similiar to Yellow gold?
how is this dosed?
sign me up for a few pounds
prld2gr8ns
Idiot Savant
Perhaps large was an overstatement.
WhatsaRoid?
Board Sponsor
dsade said:
You are the man...hell yea I been waiting all this time for my god damn ap so I can place a order. **** it ima buy this..dsade did it again.
P01Shooter
New member
dsade said:
Have you guys thought about volume discounts? There are several herbs I'd be willing to get a kilo or 500 g's if it was worth it.
johnfaceman
Active member
P01Shooter said:
Im with you on that one brotha. or at least like 200 grams :hot:
Mulletsoldier
Binging on Pure ****ing Rage
I do not wish to cause any controversy or argument so I will make this brief. Bulk Berberine is not Anabolic Pump, Phellodendron contains Berberine, though our extract does not utilize AMPK activation, and does not pose a detriment to protein synthesis
-Mullet
-Mullet
johnfaceman
Active member
Mulletsoldier said:
No controversy here :drunk: . I just want this to hold me till AP arrives. If it works well I may use it in conjunction with a lower dose of AP to alleviate the cost.
WhatsaRoid?
Board Sponsor
johnfaceman said:
i feel the same way...
dsade
NutraPlanet Fanatic
Berberine was requested as something that would stack well with DCP.wojo said:
I also went over my supplier's overstock list, and he had it for me.
As for the jabs being thrown our way that we are aching to copy USP...ridiculous. I can do my own research and design, as I have already proven.
johnfaceman
Active member
dsade said:
Yea... I think you reaking HAVOC, and the beauty of DCP will prove that. Anyway AP is being reformulated for any of those thinking it will be a copy.
dsade
NutraPlanet Fanatic
Derived from the Vinegar discussion at M&M, and the article cited:
Cellular Basis of Exercise-induced Changes in Substrate Metabolism
Finally, Neil Ruderman, MD, PhD, of the Boston University School of Medicine, a leader in the enzymology of muscle metabolic pathways, discussed the latest information on the cellular basis for exercise-induced changes in substrate metabolism.[7] Dr. Ruderman addressed the regulatory events that allow the muscle cell to utilize glucose or fatty acids at rest and during exercise, and he focused particularly on the role of AMP-activated protein kinase (AMPK) in fatty acid oxidation.
Skeletal muscles consume 80% to 90% of whole body oxygen utilized during exercise. Their choice of substrate for fuel differs during rest and exercise in normal persons. At rest (while fasting) about 90% of fuel consumption is fatty acid-derived and about 10% is carbohydrate-derived. But with moderate exercise, there are substantial increases in both fatty acid and carbohydrate oxidation. How do these shifts occur? There is an important molecular sensor that regulates the change the level of AMP in the cell, which reflects a decrease in the fuel supply.
During exercise, as a result of increased glucose uptake and glycogenolysis, glucose-6-phosphate increases in muscle cells. Normally it is not permitted to accumulate because pyruvate dehydrogenase is activated within seconds, resulting in increased flux through the Krebs cycle leading to increased glucose oxidation. Fatty acids are likewise oxidized but via a different pathway under different regulation. Lipolysis during exercise leads to increased delivery of free fatty acids to muscle cells. These are taken up by the cells, initially bound to a fatty acid binding protein, and then acted on by fatty acyl-CoA synthase to produce long chain fatty acyl-CoA.
A crucial next step is the activation of carnitine palmitoyl transferase I (CPT I) to shuttle the fatty acyl-CoA into the mitochondria for oxidation. CPT I is inhibited by malonyl-CoA, which is synthesized by the action of acetyl-CoA carboxylase (ACC), ACC is regulated positively by increased citrate (an allosteric activator that accumulates in the presence of insulin and glucose) and negatively by AMPK. Citrate activates ACC, while AMPK phosphorylates and inhibits ACC in a manner that supersedes the effect of insulin and glucose. A third regulator of malonyl-CoA is malonyl-CoA decarboxylase, the activity of which is also increased by AMPK, and which decreases malonyl-CoA levels in the cytosol.
To put these events in a physiologic context: during feeding, in the presence of insulin and glucose, malonyl-CoA accumulates and inhibits CPT I, thus inhibiting fatty acid oxidation. Conversely, when the muscle cell is deprived of glucose, or when it is contracting, malonyl-CoA decreases due to increased AMPK activity (resulting from low fuel supply and increased cellular AMP) as well as increased malonyl-CoA decarboxylase activity -- fatty acyl-CoA can then be transferred to the mitochondrion for oxidation.
So, as a result of AMPK activation during muscle contraction, the activity of ACC goes down and the activity of malonyl-CoA decarboxylase goes up, and they remain in this state for some time after the contraction. During this time the concentration of malonyl-CoA presumably remains low, permitting enhanced fatty acid oxidation. This mechanism may be a major pathway of enhancing lipid oxidation after exercise. There are also other amplifying effects of this mechanism. For instance, AMPK can also phosphorylate and inhibit glycerol phosphate acyl-transferase, an early step in forming diacylglycerol and triglycerides. It would be beneficial to prevent the accumulation of these lipid moieties in the muscle cell, inasmuch as increases in muscle diacylglycerol, triglyceride, fatty acyl-CoA, and the resultant activation of protein kinase C isoforms, are associated with insulin resistance. Furthermore, data from research by Goodyear and colleagues[8] at the Joslin Diabetes Center, Boston, show AMPK activity enhances glucose uptake into muscle cells.[8]
These data underscore the importance of effective lipid oxidation in response
taken from:Invalid Link Removed
Correct me, then, if I am wrong...but a DCP/SesaThin/Berberine dose before workout, then Anti-Oxidants/HCA/Vinegar/citrate post workout would seem to be an extremely potent Recomp protocol?
Thoughts?
Cellular Basis of Exercise-induced Changes in Substrate Metabolism
Finally, Neil Ruderman, MD, PhD, of the Boston University School of Medicine, a leader in the enzymology of muscle metabolic pathways, discussed the latest information on the cellular basis for exercise-induced changes in substrate metabolism.[7] Dr. Ruderman addressed the regulatory events that allow the muscle cell to utilize glucose or fatty acids at rest and during exercise, and he focused particularly on the role of AMP-activated protein kinase (AMPK) in fatty acid oxidation.
Skeletal muscles consume 80% to 90% of whole body oxygen utilized during exercise. Their choice of substrate for fuel differs during rest and exercise in normal persons. At rest (while fasting) about 90% of fuel consumption is fatty acid-derived and about 10% is carbohydrate-derived. But with moderate exercise, there are substantial increases in both fatty acid and carbohydrate oxidation. How do these shifts occur? There is an important molecular sensor that regulates the change the level of AMP in the cell, which reflects a decrease in the fuel supply.
During exercise, as a result of increased glucose uptake and glycogenolysis, glucose-6-phosphate increases in muscle cells. Normally it is not permitted to accumulate because pyruvate dehydrogenase is activated within seconds, resulting in increased flux through the Krebs cycle leading to increased glucose oxidation. Fatty acids are likewise oxidized but via a different pathway under different regulation. Lipolysis during exercise leads to increased delivery of free fatty acids to muscle cells. These are taken up by the cells, initially bound to a fatty acid binding protein, and then acted on by fatty acyl-CoA synthase to produce long chain fatty acyl-CoA.
A crucial next step is the activation of carnitine palmitoyl transferase I (CPT I) to shuttle the fatty acyl-CoA into the mitochondria for oxidation. CPT I is inhibited by malonyl-CoA, which is synthesized by the action of acetyl-CoA carboxylase (ACC), ACC is regulated positively by increased citrate (an allosteric activator that accumulates in the presence of insulin and glucose) and negatively by AMPK. Citrate activates ACC, while AMPK phosphorylates and inhibits ACC in a manner that supersedes the effect of insulin and glucose. A third regulator of malonyl-CoA is malonyl-CoA decarboxylase, the activity of which is also increased by AMPK, and which decreases malonyl-CoA levels in the cytosol.
To put these events in a physiologic context: during feeding, in the presence of insulin and glucose, malonyl-CoA accumulates and inhibits CPT I, thus inhibiting fatty acid oxidation. Conversely, when the muscle cell is deprived of glucose, or when it is contracting, malonyl-CoA decreases due to increased AMPK activity (resulting from low fuel supply and increased cellular AMP) as well as increased malonyl-CoA decarboxylase activity -- fatty acyl-CoA can then be transferred to the mitochondrion for oxidation.
So, as a result of AMPK activation during muscle contraction, the activity of ACC goes down and the activity of malonyl-CoA decarboxylase goes up, and they remain in this state for some time after the contraction. During this time the concentration of malonyl-CoA presumably remains low, permitting enhanced fatty acid oxidation. This mechanism may be a major pathway of enhancing lipid oxidation after exercise. There are also other amplifying effects of this mechanism. For instance, AMPK can also phosphorylate and inhibit glycerol phosphate acyl-transferase, an early step in forming diacylglycerol and triglycerides. It would be beneficial to prevent the accumulation of these lipid moieties in the muscle cell, inasmuch as increases in muscle diacylglycerol, triglyceride, fatty acyl-CoA, and the resultant activation of protein kinase C isoforms, are associated with insulin resistance. Furthermore, data from research by Goodyear and colleagues[8] at the Joslin Diabetes Center, Boston, show AMPK activity enhances glucose uptake into muscle cells.[8]
These data underscore the importance of effective lipid oxidation in response
taken from:Invalid Link Removed
Correct me, then, if I am wrong...but a DCP/SesaThin/Berberine dose before workout, then Anti-Oxidants/HCA/Vinegar/citrate post workout would seem to be an extremely potent Recomp protocol?
Thoughts?
johnfaceman
Active member
Not the smartest person here, but it sounds pretty damn spot on to me. I might give it a run when I can buy some DCP samples and let you know.
johnfaceman
Active member
Whats the good news?!? :blink:
johnfaceman
Active member
johnfaceman said:
Bump, was hoping to make an order soon.
johnfaceman
Active member
Jayhawkk said:
Now we all know thats not true. D was told to hold a couple kilos for me :twisted:
johnfaceman
Active member
dsade said:
When will you have that little bit available. Im ready to buy.
johnfaceman
Active member
stryder said:Invalid Link Removed now in stock
Got some coming my way! :bb2: