Wednesday, January 10, 2018

"Oral administration of adenosine is effective for improving metabolic syndrome-related parameters [...] [and] may prevent the progression of the metabolic syndrome" - PubMed - NCBI

ADENOSINE MONOPHOSPHATE:

What CAN'T It Do? 

Just yesterday we shared research that shows Adenosine Monophosphate is beneficial for activating the molecular pathway responsible for energy management: AMPK. Well the good news just keeps rolling in.

To further test the metabolic impact of supplemental AMP, researchers introduced AMP to a group of rats fed a high-fat diet. They found that the groups receiving regular doses of AMP had significant reductions in blood pressure, LDL Cholesterol (bad cholesterol), plasma glucose and insulin levels compared to placebo. Furthermore, levels of urinary 8-OHd, a well-established indicator of oxidative stress, were nearly halved in the AMP groups compared to placebo.

The researchers used rats known as SHRSP (spontaneously hypertensive stroke-prone) because they are known to exhibit spontaneous hypertension, hyperlipidaemia and insulin resistance. The efficacy of AMP in treating these biologically fragile specimens gives promise to the use of AMP as an effective therapy for similarly compromised human patients, such as those suffering from one or more of the following conditions: Obesity, Hypertension, Insulin Resistance/Pre-diabetes, etc.
Br J Nutr. 2010 Jul;104(1):48-55. doi: 10.1017/S0007114510000255. Epub 2010 Feb 23.

Anti-metabolic syndrome effects of adenosine ingestion in stroke-prone spontaneously hypertensive rats fed a high-fat diet. 

Ardiansyah, Shirakawa H, Sugita Y, Koseki T, Komai M.

 


Abstract

We have demonstrated previously that both acute and chronic oral administration of adenosine have novel functions such as anti-hypertensive effects and improved hyperlipidaemia in stroke-prone spontaneously hypertensive rats (SHRSP) fed a normal diet. The purpose of the present study was to investigate the effect of adenosine administration on metabolic syndrome-related parameters in SHRSP fed a high-fat diet. Six-week-old rats were divided into three groups, and were administered either water (control) or adenosine (10 or 100 mg/l) for 8 weeks. During this period, the rats had free access to a high-fat diet based on AIN-93M. The results showed that hypertension, plasma lipid, NO, insulin, glucose and urinary 8-hydroxy-2'-deoxyguanosine levels improved significantly in both adenosine groups. The mRNA expression levels of genes involved in anti-oxidative activity and adenosine receptors were also altered in the adenosine groups. Administration of adenosine also increased plasma adiponectin levels, accompanied by upregulation of mRNA expression level of adiponectin and adiponectin receptor 1 in perirenal fat and adiponectin receptor 2 in the liver. In conclusion, oral administration of adenosine is effective for improving metabolic syndrome-related parameters in SHRSP, and accordingly it may prevent the progression of the metabolic syndrome.

https://www.ncbi.nlm.nih.gov/pubmed/20175942 
REMEMBER: For the highest quality form of AMP, ask your doctor about MYODEN from Legere Pharmaceuticals.

Tuesday, January 9, 2018

BURN fat, don't store it!

Researchers have discovered a molecular pathway for stimulating the body to burn fat. This discovery could be helpful in fighting obesity, diabetes and cardiovascular disease. 

To test this pathways, mice that have been genetically engineered to over-express this molecular pathway were fed a high-fat diet for 14 weeks. At the end of the study, the normal mice had rapidly gained weight but the genetically modified mice remained slim and did not have the same elevated insulin and triglyceride levels that the normal mice did. Further analysis found that the genetically engineered mice were in fact burning more fat.

What is this new miraculous molecular pathway responsible for these result? AMPK (Adenosine Monophosphate-Activated Protein Kinase). Researchers found that by boosting AMPK activity, the proteins PGC-1α and ERRα were activated - increasing the number and work rate of the cells' mitochondria. The end result is a metabolic reprogramming that switches the body from a fat storage machine to a fat burning machine.

Activated AMPK promotes all the processes needed to maintain a youthful profile. To further test the anti-aging properties of AMPK, researchers used fruit flies that, similar to the aforementioned mice, were genetically engineered to have higher levels of AMPK activity. The research found that the modified flies lived up to one-third longer than normal flies. "The life span benefit of these mutations depends upon increased AMP:ATP and ADP:ATP ratios and adenosine monophosphate-activated protein kinase (AMPK). Transgenic expression of AMPK in adult fat body or adult muscle, key metabolic tissues, extended life span" (Stenesen, 2013).

The mechanism used to engineer increased AMPK activity in these test subjects was to genetically modify the flies to produce more adenosine monophosphate (AMP). As the name implies, increased levels of AMP results in increased levels of AMPK. However, one does not require genetic mutations to achieve the results of increased AMPK activity. Researchers have now confirmed that consistent dosages of oral AMP results in increased AMPK activity. In a study using lab rats fed supplemental AMP, "AMP effectively improved hypertension, plasma triglyceride, and HDL-cholesterol, glucose, kidney function parameters, hepatic lipid, enhances plasma nitric oxide, and plasma adiponectin..." (Ardiansyah, 2011). The researchers found that AMP up-regulated mRNA expression levels, affecting genes involved in B-oxidation, fatty acid synthesis, and AMPK. 

It is clear that AMPK activity is desirable for reducing the unwanted effects of aging. AMPK activity can be increased through exercise and proper nutrition however as we age, AMPK activity declines. This decline can be reduced and possibly even reversed through pharmacologic AMPK activation such as that achieved through supplemental oral AMP.

There are many products that claim to be AMPK activators, but only AMP has been proven in laboratory settings to directly increase AMPK activity via oral administration. For the highest quality form of AMP, ask your doctor about MYODEN from Legere Pharmaceuticals.


Myoden Spray


Ming, Yan., et. al. (2016). Chronic AMPK activation... Genes & Development.
Stenesen, D., Suh, JM., Seo, J., Yu, K., Lee, K.S., Min, K.J., & Graff, J.M. (2013). Adenosine nucleotide biosynthesis and AMPK regulate adult life span and mediate the longevity benefit of caloric restriction in flies. Cellular Metabolism. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/23312286
Ardiansyah, Shirakawa, D., Koseki, H., Saori, T., Yoshinobu, A., & Michio, K. (2011). Novel Effect of Adenosine 5′-Monophosphate on Ameliorating Hypertension and the Metabolism of Lipids and Glucose in Stroke-Prone Spontaneously Hypertensive Rats. Journal of Agricultural and Food Chemistry.

Wednesday, January 3, 2018

Hydroxycitric Acid - Carb Blocker

Hydroxycitric acid is found in the rind of Garcinia cambogia fruit. Research has found that this compound acts as a potent competitive inhibitor of the enzyme ATP Citrate Lyase. ATP Citrate Lyase plays a crucial role in carbohydrate metabolism and the Kreb's cycle as an intermediary in the creation of cholesterol and fat. 





Learn more about the weight loss benefits of Hydroxycitric acid in our white paper: WHITE PAPER




Thursday, November 30, 2017

AMPK - An Ideal Target For Weight Loss & Anti-Aging

The evolution of medical science has revealed that many of the common symptoms of aging may be caused by a reversible failure of cellular mechanics. One such mechanic that has been the target of anti-aging research is a cellular enzyme known as adenosine monophosphate-activated protein kinase (AMPK).

AMPK is activated in the presence of rising levels of Adenosine Monophosphate (AMP). AMPK activation increases fatty acid oxidation and glucose transport, releasing additional energy from stored fats and sugars. In essence, activated AMPK promotes energy-releasing processes while suppressing energy-storing processes. As a result, organisms with high AMPK activity tend to be more lean, with relatively low blood sugar and fat levels, and a very low risk of heart disease, diabetes, and other metabolic disorders.




Activated AMPK promotes all the processes needed to maintain a youthful profile. However, AMPK activity fades with age. As previously mentioned, AMPK is activated in the presence of increased AMP. Therefore, to test the anti-aging properties of AMPK, researchers used fruit flies that were genetically engineered to synthesize higher levels of AMP. The research found that the modified flies lived up to one-third longer as a result of increased AMPK activity. "The life span benefit of these mutations depends upon increased AMP:ATP and ADP:ATP ratios and adenosine monophosphate-activated protein kinase (AMPK). Transgenic expression of AMPK in adult fat body or adult muscle, key metabolic tissues, extended life span" (Stenesen, 2013).

Luckily, AMPK can be activated without genetic manipulation. Researchers have now confirmed that consistent dosages of oral AMP results in increased AMPK activity. In a study using lab rats fed supplemental AMP, "AMP effectively improved hypertension, plasma triglyceride, and HDL-cholesterol, glucose, kidney function parameters, hepatic lipid, enhances plasma nitric oxide, and plasma adiponectin..." (Ardiansyah, 2011). The researchers found that AMP up-regulated mRNA expression levels, affecting genes involved in B-oxidation, fatty acid synthesis, and AMPK. 


 

It is clear that AMPK activity is desirable for reducing the unwanted effects of aging. AMPK activity can be increased through exercise and proper nutrition however as we age, AMPK activity declines. This decline can be reduced and possibly even reversed through pharmacologic AMPK activation such as that achieved through supplemental oral AMP.




Sources:

Stenesen, D., Suh, JM., Seo, J., Yu, K., Lee, K.S., Min, K.J., & Graff, J.M. (2013). Adenosine nucleotide biosynthesis and AMPK regulate adult life span and mediate the longevity benefit of caloric restriction in flies. Cellular Metabolism. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/23312286

Ardiansyah, Shirakawa, D., Koseki, H., Saori, T., Yoshinobu, A., & Michio, K. (2011). Novel Effect of Adenosine 5′-Monophosphate on Ameliorating Hypertension and the Metabolism of Lipids and Glucose in Stroke-Prone Spontaneously Hypertensive Rats. Journal of Agricultural and Food Chemistry.

Linton, R. (2015). AMPK and Aging. Life Extension.

Tuesday, November 14, 2017

Neurohormone signaling and obesity.

When food enters the stomach, your body responds by sending signals via hormones to the brain. The intricate circuitry between the gut and brain controls appetite and satiety. After a meal, levels of hormones such as CCK rise leading to feelings of satiety. Compared with lean subjects, overweight patients have lower post-meal levels of CCK: a possible explanation for overeating and reduced satisfaction after a meal.

Studies have shown that levels of the appetite regulating hormone CCK remain suppressed even after weight loss. Reductions of this hormone can persist up to one year after weight loss, promoting increased appetite and decreased satiety; potentially leading to overeating and weight regain.

L-phenylalanine is a naturally occurring amino acid which has been shown to increase CCK. A double-blind study found that L-phenylalanine led to an increase of CCK levels by more than 5X base levels. There were no negative side effects. Furthermore, the L-phenylalanine group saw a significant reduction in caloric intake, giving evidence to the use of L-phenylalanine to control appetite, especially in cases where CCK production is otherwise suppressed.



Smith, A. (2017). Neurohormonal effects on obesity. Bariatric Times. Retreived from: http://bariatrictimes.com/neurohormonal-effects-obesity-nov2017/

Ballinger, AB., Clark, ML. (1994). L-phenylalanine releases cholecystokinin (CCK) and is associated with reduced food intake in humans. Metabolism. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/8201963

Tuesday, November 7, 2017

Fish Oils: Why Omega 3 should be a staple of your weight loss program.

Omega 3 fatty acids have long been known for their benefits relating to heart disease, but they are important for so much more! Optimizing your omega-3 is a truly foundational component of good health.



Fish Oil Supplements Decrease Your Appetite.
If you want to stay full longer between meals, popping a couple of fish oil capsules after you eat may help. A 2008 study found that obese people receiving supplements of omega-3 fatty acids while following a weight loss program experienced a feeling of fullness for longer.

Source: https://www.nutraingredients.com/Article/2008/06/25/Omega-3-boosts-satiety-during-weight-loss-study

Fish Oil Makes Your Diet and Workout Program More Effective.
The results of one study demonstrated that fish oil supplementation significantly increased resting metabolic rate, energy expenditure during exercise, and the rate of fat oxidation during rest and during exercise. In addition, fish oil consumption lowered triglyceride levels and increased lean mass, while no changes occurred in the placebo group.

Source: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0144828

Thursday, November 2, 2017

Vitamin C and Weight Loss: The Stress Connection

Being under stress causes a release of the hormone cortisol. Cortisol's functions include blood pressure regulation, glucose metabolism, blood sugar maintenance, and immune system support. During a stressful event this has positive effects including a higher pain threshold and a rush of energy. However, when your body is constantly producing an abnormally high amount of cortisol, it can disrupt your normal cortisol production and have a negative impact on your health.
Excess cortisol stimulates glucose production leading to a release of insulin. These internal activites result in an increase in appetite. Additionally, the excess glucose is converted to and stored as fat. Some studies have shown that excess cortisol not only increases fat storage, it can also effect where the fat is stored. Researchers believe that cortisol specifically leads to an increase of abdominal fat.


It is possible to keep excess cortisol in check with the proper nutrients, such as vitamin C. Studies have shown that supplementing with between 500mg and 1000mg of vitamin C daily can help reduce cortisol levels post-exercise compared with placebo. Additionally, as an anti-oxidant, vitamin C may be effective for reducing oxidative damage from free radicals produced when cortisol levels are high.