Fat Metabolism Starts With the Amino Acid L-carnitine
L-carnitine is amino acid essential for the metabolism of fats into a form of energy necessary for extended aerobic activity. Originally discovered in Russia, and Germany a year later, the structural formulation of carnitine, as it is correctly known, was determined in 1927, although it is physiological and biochemical activity was not understood until the 1960s.
The amino acid is biosynthesized in the liver and kidneys from lysine and methionine. The vitamins niacin, B6, C and iron are essential for this reaction to take place. However, the supply of L-carnitine has to be supplemented by the diet, good sources being dairy products, red meat, nuts and seeds, pulses and fruits such as apricots, bananas and avocado. Most of the L-carnitine supply of the body is stored within the muscle tissue. However, it is not unusual for conditions to arise making it difficult for the body to obtain all the carnitine required.
L-carnitine enables fatty acids to be transported into the mitochondria, where cell metabolism occurs. The biochemistry is discussed below, although in simple terms the amino acid allows body fats, in the form of triglycerides, to be made more readily available for the generation of energy required for extended exertion. In this way, body fats can be used for energy and the supplies of glycogen stored by the liver can be retained for emergency use.
By providing the energy for endurance and stamina in this way, carnitine makes use of an otherwise unavailable energy source, and has the added benefit of reducing body fat stores and reducing strain on the heart.
Although there is generally a plentiful supply of L-carnitine available in a healthy diet, supplementation can ensure that a deficiency does not occur. Supplements are available in the form of L-carnitine or its acetylated derivative, acetyl L-carnitine.
In order for fatty acids to be used in the production of energy, their long-chain acetyl groups have to get inside the mitochondria where they are oxidized to the acetate to be used for the production of energy via the Citric Acid or Krebs cycle.
In order for the biochemistry to take place, fatty acids must be rendered suitable for binding to the carnitine molecule. The chemical grouping with a good affinity for L-carnitine is the acetyl or acetyl group, available in the molecule acetyl coenzyme A (CoA). The free fatty acid, therefore, is attached to coenzyme-A by means of a thioester bond, catalyzed by means of the enzyme fatty acetyl-CoA synthetase. The reaction is then completed by means of in organic pyrophosphatase.
In this way, the fatty acid in the form of an acetyL-carnitine derivative can be transported through the mitochondrial wall. This transportation takes place by means of several steps. These are:
1. As explained, the acetyl-CoA is attached to L-carnitine by means of the enzyme carnitine acetyltransferase I. This enzyme is conveniently located on the outer mitochondrial membrane.
2. The enzyme carnitine-acetylcarnitine translocase helps the acetyL-carnitine through the membrane.
3. Another enzyme, carnitine acetyltransferase II, located on the inner mitochondrial membrane, converts the acetyL-carnitine to acetyl-CoA, liberating the carnitine which returns to the muscle mass.
L-carnitine is the only known substance that allows fatty acids to cross the mitochondrial membrane, and therefore deficiencies must be avoided.
Another way in which carnitine is used in energy production is in the Krebs cycle itself. Part of this cycle involves the conversion of guanine diphosphate to the higher energy form guanine triphosphate. In this way energy can be stored in much the same way as it is in the conversion of ADP to ATP. Succinyl CoA is involved in this conversion, and one of the by-products of it is a corresponding succinate, that is then converted to a fumarate by the action of L-carnitine fumarate. Carnitine, therefore, has two parts to play in the production of long-term energy from the fatty acids contained in body fats.
Since the fatty acid triglycerides contained in body fats are a major source of energy in the heart and skeletal muscles, it is easy to understand how L-carnitine is believed to lead to the increased energy levels required for stamina and staying power. A major reason for its effect on longer-term or extended energy requirements is that in enabling stored body fats to be used for immediate and longer-term energy requirements, L-carnitine allows emergency glycogen stores to be retained for use once immediate fatty acid supplies or those of carnitine have been depleted, and so allows the energy supply to be extended even farther. Research has also suggested that the amino acid can possibly be used to treat liver and kidney disease, diabetes and chronic fatigue syndrome.
As with many supplements, the question is often asked how does L-carnitine work in practice as opposed to the claims made for it by the supplement providers? Recent research indicates mixed results, but sufficient to justify its use. It is generally accepted that a supplement is necessary when there is a deficiency, but once that deficiency has been corrected further intake is unnecessary. However, it is also believed that during long and extended periods of exercise a carnitine deficiency does occur as L-carnitine is used up, and the supplement is necessary to ensure sufficient energy supply throughout the period of exercise.
There has also been a case reported in the Journal of Clinical Neurology (Negoro, Tsuda, Kato & Morimatsu, 1995) where a deficiency, caused by anorexia nervosa damaging the liver to the extent that it was unable to synthesize L-carnitine, was remedied by means of an oral supplement. Studies on endurance athletes have been mixed, ranging from no effect to L-carnitine being found to promote weight loss.
Carnitine has no unknown harmful side effects, and has been studied for medical applications other than as an energy supplement. For example it possesses extensive antioxidant properties, and can be used as a supplement against oxidative stress and the prevention of the lipid peroxidation that is a precursor to atherosclerosis.
Its use in osteoporosis and reducing bone mass is also being studied. The concentration of L-carnitine diminishes with age, and affects fatty acid metabolism in a number of tissues. Bones are particularly affected since they require continuous reconstruction. Without detailing the biochemistry involved in this, administration of carnitine helps to reduce the speed by which this occurs. Trials are so far been carried out only on animals.
In studies on both healthy volunteers and patients with type II diabetes, L-carnitine was found to improve storage of glucose in both groups, although its oxidation increased only in the group with diabetes. Other studies carried out include improving the function of neurotransmitters in the brains of elderly patients and in the treatment of Alzheimer’s and Parkinson’s disease, and other neurological disorders.
In conclusion then, although the jury is out on the use of L-carnitine is an energy-giving or weight-loss supplement, it appears to be effective where the body’s stores of carnitine could be depleted such as with long-term exercise, natural deficiencies or deficiencies caused through age. It is also under study in the treatment of various medical conditions. On balance, it would appear that the prospective benefits of L-carnitine render it worthy of use.
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