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Then In a few days I should feel better.. The reason for the four stars - price! After surgery we were informed the appendix had burst. Its function is enhanced by electrolytes, a glycogen complex, and vitamins. I would take it again if I believed I ws getting the real stuff. The active ingredient in Phentermine is phentermine hydrochloride.

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This species exists is various modifications tautomers in solution. Creatine is found in vertebrates where it facilitate recycling of adenosine triphosphate ATP , the energy currency of the cell, primarily in muscle and brain tissue.

Creatine also acts as a buffer. Creatine is a derivative of the guanidinium cation. A cyclic form of creatine, called creatinine , exists in equilibrium with its tautomer and with creatine. Creatine undergoes phosphorylation , by the action of creatine kinase to give phosphocreatine.

The phosphate group is attached to an NH center of the creatine. The P-N bond is highly reactive. Creatine was first identified in when Michel Eugène Chevreul isolated it from the basified water-extract of skeletal muscle.

In , creatine was shown to exist in equilibrium with creatinine. This result pointed to the ability of the body to store creatine, which in turn suggested its use as a dietary supplement. The discovery of phosphocreatine [5] [6] was reported in Creatine synthesis primarily occurs in the liver and kidneys. Creatine is not an essential nutrient [13] as it is naturally produced in the human body from the amino acids glycine and arginine.

In the first step of the biosynthesis these two amino acids are combined by the enzyme arginine: Creatine itself can be phosphorylated by creatine kinase to form phosphocreatine , which is used as an energy buffer in skeletal muscles and the brain. Synthesis primarily takes place in the kidney and liver, with creatine then being transported to the muscles via the blood. The majority of the human body's total creatine and phosphocreatine stores is located in skeletal muscle, while the remainder is distributed in the blood , brain, and other tissues.

However, subjects happened to show the same levels after using supplements. Creatine, which is synthesized in the liver and kidneys , is transported through the blood and taken up by tissues with high energy demands, such as the brain and skeletal muscle, through an active transport system. Additionally, in most muscles, the ATP regeneration capacity of CK is very high and is therefore not a limiting factor. Genetic deficiencies in the creatine biosynthetic pathway lead to various severe neurological defects.

Deficiencies in the two synthesis enzymes can cause L-arginine: Both biosynthetic defects are inherited in an autosomal recessive manner. A third defect, creatine transporter defect , is caused by mutations in SLC6A8 and inherited in a X-linked manner. This condition is related to the transport of creatine into the brain. Such a reaction happens when grilling or pan-frying meat.

Use of creatine by healthy adults in normal dosages does not harm kidneys; its effects on the kidney in elderly people and adolescents were not well understood as of People with kidney disease, high blood pressure, or liver disease should not take creatine as a dietary supplement. One well-documented effect of creatine supplementation is weight gain within the first week of the supplement schedule, likely attributable to greater water retention due to the increased muscle creatine concentrations.

A systematic review discredited concerns that creatine supplementation could affect hydration status and heat tolerance and lead to muscle cramping and diarrhea. Creatine taken with medications that can harm the kidney can increase the risk of kidney damage: Creatine has a fairly short elimination half-life, averaging just less than 3 hours, so to maintain an elevated plasma level it would be necessary to take small oral doses every 3—6 hours throughout the day.

As with most supplements, each person has their own genetic "preset" amount of creatine they can hold. The rest is eliminated as waste. Creatine supplementation appears to increase the number of myonuclei that satellite cells will 'donate' to damaged muscle fibers , which increases the potential for growth of those fibers. This increase in myonuclei probably stems from creatine's ability to increase levels of the myogenic transcription factor MRF4. Creatine supplements are marketed in ethyl ester , gluconate , monohydrate , and nitrate forms.

The most prevalent of these contaminants was creatinine , a breakdown product of creatine also produced by the body. Heavy metals contamination was not found to be a concern, with only minor levels of mercury being detectable. Two studies reviewed in found no impurities. In , Harvard University researchers Otto Folin and Willey Glover Denis found evidence that ingesting creatine can dramatically boost the creatine content of the muscle. The substance creatine is naturally formed in vertebrates.

While creatine's influence on physical performance has been well documented since the early twentieth century, it came into public view following the Olympics in Barcelona. An August 7, article in The Times reported that Linford Christie , the gold medal winner at meters, had used creatine before the Olympics.

An article in Bodybuilding Monthly named Sally Gunnell , who was the gold medalist in the meter hurdles, as another creatine user. In addition, The Times also noted that meter hurdler Colin Jackson began taking creatine before the Olympics. At the time, low-potency creatine supplements were available in Britain, but creatine supplements designed for strength enhancement were not commercially available until when a company called Experimental and Applied Sciences EAS introduced the compound to the sports nutrition market under the name Phosphagen.

It is ineffective as a treatment for amyotrophic lateral sclerosis. A meta-analysis found that creatine treatment increased muscle strength in muscular dystrophies, and potentially improved functional performance.

Creatine's impact on mitochondrial function has led to research on its efficacy and safety for slowing Parkinson's disease. As of , the evidence did not provide a reliable foundation for treatment decisions, due to risk of bias, small sample sizes, and the short duration of trials.

From Wikipedia, the free encyclopedia. This is the latest accepted revision , reviewed on 12 September

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