# The adventures of Judo Josh



## judojosh (Aug 11, 2011)

This is not going to be a typical log. It wil not be updated often except with notes on dietary, training and supplement changes. Basically I love to experiment and try new things out. One of my favorite quotes is : 



> Life is an experiment. The more experiments you make the better you become - Ralph Waldo Emerson


 
I don't like to blindly follow advice or suggestions I like to try and figure out why something works and then try it on myself to see how my body handles it. So that is going to be the purpose of the log. My views on diet, supplementation and training are forever evolving and changing. The more I experiment with various theories the more I learn about myself and change or tweak the way I view things. So the goal of this journal is to detail all those various ideologies. There are no universal diets or training techniques, one must experiment to find what works for them and thats what this journal will be about.


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## judojosh (Aug 13, 2011)

I am taking the week to deload and get some rest. During this time I am going to figure out what I am going to do for the next 12 weeks. The overall goal and focus is going to be fat loss. Currently I am at 188lbs and want to reach 170lbs with as little strength loss as possible. 

Sometime today I am going to post up why i believe in fasted training for weight loss and how I plan on furthering that fat loss with supplementation. Then later on in the week I will put up my training and my diet.

As always I am appreciative of feedback. Let me know what you guys think. If I am wrong or off base about something then please correct me and explain how and why I am wrong.


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## judojosh (Aug 13, 2011)

*First up*

I have always been a fan of fasted training. What first introduced me to this was a couple post by Mulletsolider on the topic of fasted training along with anabolic pump and the possible fat loss benfits.
I tried this and had great results with it but wanted to figure out more of why it worked and see if I could duplicate it with another cheaper product and in comes Berberine. 
One of the reason I believe why Anabolic Pump was successful for weightloss when combined with fasted training was Anbolic Pumps ability to activate AMPk.


> Anabolic Pump is often conceptualized as merely a supplement of glucose homeostasis. While that's true in part, its true identity is one of energy metabolism as a whole; specifically, modulating energy expenditure and transfer in both fat and muscle cells, via the modulation of energy storage and production mechanisms.
> During a long bout of exercise (i.e., an hour long resistance training session) your body's energy homeostasis mechanisms need to take on a more oxidative (the B-oxidation of fatty acids) as opposed to glycolytic (GLUT4 translocation and glucose storage) role. This is due in part to the inability of the body to produce the fuel (glucose) for anabolic processes at the rates needed for anaerobic exercise. In response, your body has in place several mechanisms which prevent the accumulation and synthesis of triglycerides and lipids, and release them into the bloodstream to be oxidized.
> These lipolytic processes actually contribute to the majority of energy transaction in a bout of anaerobic exercise - the oxidation of fatty acids and plasma triglycerides, primarily, provide the energy for resistance training.
> The reason I mention all this is Anabolic Pump's fascinating ability to regulate one of the vanguards of oxidative and glycolytic energy consumption - AMPk. AMPk works as an essential gate-keeper of energy production, reacting to extracellular fluctuations of various downstream energy messengers (*AMP:ATP ratio* included). Its activation is responsible for various roles, including all of the above mentioned.
> ...


So my theory is that the reason Anabolic Pump was successful for weight loss when combined with fasted training was because it activated AMPk.
How does AMPk help with fat loss?


> The role of AMPK, both in energy regulation and fat loss, should be highlighted more often. In particular, * AMPK activation (either due to insulin sensitizers, insulin-independent glucose-disposal agents*, PPAR-gamma activators, adipokines such as leptin and adiponectin, stress, or exercise), has short term and long(er) term effects. Short-term, AMPK activation *stimulates cells to switch from active ATP consumption (synthesis of fatty acids and glycerol) to active ATP production *(oxidation of fatty acids and glucose). Longer-term, AMPK activation impacts protein and insulin syntheses, gene expression, and appetite regulation. These longer-term effects not only have significance for metabolic processes in muscle cells and adipose tissue, but also in liver, heart, and pancreatic cells. The fat loss effects can be traced to the impact of AMPK activation on insulin metabolism and oxidation of fatty acids. In particular, by stimulating the translocation the GLUT-1 and GLUT-4 proteins, AMPK activation enhances glucose uptake, *leading to enhanced glycolysis and elevated ATP production.* Furthermore, by inhibiting the action of the enzyme, hormone sensitive lipase (HSL), AMPK activation *ensures that the HSL-induced rate of release of fatty acids from triglycerides (that would normally induce higher ATP levels due to oxidized fatty acids) does not exceed the rate of fatty acid oxidation*. This serves to hinder fat accumulation. Along these lines, the impact of AMPK activation on peroxisome proliferator-activated receptor gamma (PPAR-gamma), a receptor with primarily adipocyte domicile and activity, leads to increased insulin sensitivity and fatty-acid oxidation in hepatic and skeletal muscle cells. This occurs mainly via the action of the adipokine, adiponectin, that triggers glucose uptake and fatty acid oxidation in skeletal muscle cells, while promoting fatty acid oxidation and inhibiting gluconeogenesis in hepatic cells. In summary, AMPK activation can produce beneficial effects on fat loss via some of the mechanisms addressed earlier.


So what does have to do with Berberine?
Berberine Increases Glucose Uptake Independent of Insulin and also activates AMPk


> ???*Berberine stimulates glucose transport through a mechanism distinct from insulin*.
> Zhou L, Yang Y, Wang X, Liu S, Shang W, Yuan G, Li F, Tang J, Chen M, Chen J.
> Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
> Berberine exerts a hypoglycemic effect, but the mechanism remains unknown. In the present study, the effect of berberine on glucose uptake was characterized in 3T3-L1 adipocytes. It was revealed that berberine stimulated glucose uptake in 3T3-L1 adipocytes in a dose- and time-dependent manner with the maximal effect at 12 hours. Glucose uptake was increased by berberine in 3T3-L1 preadipocytes as well. Berberine-stimulated glucose uptake was additive to that of insulin in 3T3-L1 adipocytes, even at the maximal effective concentrations of both components. Unlike insulin, the effect of berberine on glucose uptake was insensitive to wortmannin, an inhibitor of phosphatidylinositol 3-kinase, and SB203580, an inhibitor of p38 mitogen-activated protein kinase. Berberine activated extracellular signal-regulated kinase (ERK) 1/2, but PD98059, an ERK kinase inhibitor, only decreased berberine-stimulated glucose uptake by 32%. Berberine did not induce Ser473 phosphorylation of Akt nor enhance insulin-induced phosphorylation of Akt. Meanwhile, the expression and cellular localization of glucose transporter 4 (GLUT4) were not altered by berberine. Berberine did not increase GLUT1 gene expression. However, genistein, a tyrosine kinase inhibitor, completely blocked berberine-stimulated glucose uptake in 3T3-L1 adipocytes and preadipocytes, suggesting that berberine may induce glucose transport via increasing GLUT1 activity. In addition, berberine increased adenosine monophosphate-activated protein kinase and acetyl-coenzyme A carboxylase phosphorylation. *These findings suggest that berberine increases glucose uptake through a mechanism distinct from insulin, and activated adenosine monophosphate-activated protein kinase seems to be involved in the metabolic effect of berberine*.???





> Berberine, a Natural Plant Product, Activates AMP-Activated Protein Kinase With Beneficial Metabolic Effects in Diabetic and Insulin-Resistant States
> Yun S. Lee1,2, Woo S. Kim1,2, Kang H. Kim1,2, Myung J. Yoon1, Hye J. Cho1, Yun Shen3,4, Ji-Ming Ye3, Chul H. Lee5, Won K. Oh5, Chul T. Kim5, Cordula Hohnen-Behrens3, Alison Gosby3, Edward W. Kraegen3, David E. James3, and Jae B. Kim1,2
> Berberine has been shown to have antidiabetic properties, although its mode of action is not known. Here, we have investigated the metabolic effects of berberine in two animal models of insulin resistance and in insulin-responsive cell lines. Berberine reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in db/db mice. Similarly, berberine reduced body weight and plasma triglycerides and improved insulin action in high-fat?fed Wistar rats. Berberine downregulated the expression of genes involved in lipogenesis and upregulated those involved in energy expenditure in adipose tissue and muscle. Berberine treatment resulted in increased AMP-activated protein kinase (AMPK) activity in 3T3-L1 adipocytes and L6 myotubes, increased GLUT4 translocation in L6 cells in a phosphatidylinositol 3' kinase?independent manner, and reduced lipid accumulation in 3T3-L1 adipocytes. These findings suggest that berberine displays beneficial effects in the treatment of diabetes and obesity at least in part via stimulation of AMPK activity.
> Obesity poses a serious health risk contributing to the increased prevalence of a host of other diseases including type 2 diabetes, hyperlipidemia, hypercholesterolemia, and hypertension (1,2). Peripheral insulin resistance, which is often associated with obesity, is one of the earliest detectable defects identified in individuals at risk of type 2 diabetes. For this reason, pharmacologic agents that overcome insulin resistance, so-called insulin-sensitizing agents, have received considerable attention. In recent years, several major insulin-sensitizing agents have been developed, including the thiazolidinediones (TZDs) (3) and metformin (4). Both of these agents are thought to have beneficial effects, at least in part, by activating the stress-activated kinase AMP-activated protein kinase (AMPK) (5,6). AMPK is activated under a variety of conditions that signify cellular stress, usually in response to a change in the intracellular ATP-to-AMP ratio. Active AMPK orchestrates a variety of metabolic processes, most of which lead to reduced energy storage and increased energy production. TZDs and metformin are thought to activate AMPK via discrete mechanisms; TZDs stimulate the proliferation of small adipocytes that secrete adipokines such as adiponectin, which have been shown to stimulate AMPK activity in muscle and liver cells (7). Conversely, it appears that metformin activates AMPK directly via an ill-defined mechanism (8). These studies emphasize the potential utility of targeting the AMPK pathway in the treatment of type 2 diabetes and obesity.
> The use of natural products for the treatment of metabolic diseases has not been explored in depth despite the fact that a number of modern oral hypoglycemic agents such as metformin are derivatives of natural plant products (9,10). Although several traditional medicines have been reported to have antidiabetic effects (10), the molecular targets of such compounds have not been revealed, and a careful analysis of their mode of action in animal models has not been undertaken. In the present study, we have focused on berberine because this natural product has been reported in the Chinese literature and several recent studies (11?14) to have beneficial effects in human type 2 diabetes, although its mechanism of action is not known. Here, we show that in vivo administration of berberine has insulin sensitizing as well as weight- and lipid-lowering properties in both db/db mice and in high-fat?fed rats. *Strikingly, berberine acutely stimulated AMPK activity in both myotubes and adipocytes in vitro, contributing to enhanced GLUT4 translocation in myotubes and reduced lipid mass in adipocytes.* Based on these studies, we propose that berberine may have a major application as a new treatment for obesity and/or insulin resistance in humans.???





> Berberine is a plant alkaloid used in traditional Chinese medicine and has been reported to have antihyperglycemic activity in NIDDM patients. However, the molecular basis for this action is yet to be elucidated. Here we investigate the effects and signaling pathways of berberine on L6 rat skeletal muscles. Our study demonstrates that berberine stimulates glucose uptake in a time- and dose-dependent manner. Intriguingly, *berberine-stimulated glucose uptake does not vary as insulin concentration increases*, and could not be blocked by the PI 3-kinase inhibitor wortmannin. Berberine only weakly stimulates the phosphorylation of Akt/PKB, a key molecule in the insulin signaling pathway, but strongly promotes the phosphorylation of AMPK and p38 MAPK. *The effects of berberine are not a result of pro-oxidant action, but a consequence of an increased cellular AMP:ATP ratio.* Moreover, berberine-stimulated glucose uptake is inhibited by the AMPK inhibitor Compound C and the p38 MAPK inhibitor SB202190. Inhibition of AMPK reduces p38 MAPK phosphorylation, suggesting that AMPK lies upstream of p38 MAPK. These results suggest that *berberine circumvents insulin signaling pathways and stimulates glucose uptake through the AMP-AMPK-p38 MAPK pathway,* which may account for the antihyperglycemic effects of this drug.





> Berberine has been shown to have antidiabetic properties, although its mode of action is not known. Here, we have investigated the metabolic effects of berberine in two animal models of insulin resistance and in insulin-responsive cell lines. Berberine reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in db/db mice. Similarly, berberine reduced body weight and plasma triglycerides and improved insulin action in high-fat-fed Wistar rats. *Berberine downregulated the expression of genes involved in lipogenesis and upregulated those involved in energy expenditure in adipose tissue and muscle. Berberine treatment resulted in increased AMP-activated protein kinase (AMPK) activity in 3T3-L1 adipocytes and L6 myotubes, increased GLUT4 translocation in L6 cells in a phosphatidylinositol 3' kinase-independent manner, and reduced lipid accumulation in 3T3-L1 adipocytes.* These findings suggest that berberine displays beneficial effects in the treatment of diabetes and obesity *at least in part via stimulation of AMPK activity*.


So the plan is fasted training combined with barberine should help with my fat loss goal.


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## dirtwarrior (Aug 14, 2011)

This will be an awesome thread


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## ovr40 (Aug 14, 2011)

i'll be checking it out. I think we're alike in the fact that we are, as you called it ,"carb-sensitive". We are different in the fact that, I don't care "why" x is x. I look foward to following along and learning


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