Slimming Product L-Carnitine Injection For Weight Loss

In animals, the biosynthesis of carnitine occurs primarily in the liver and kidneys from the amino acids lysine (via trimethyllysine) and methionine.

Carnitine transports long-chain acyl groups from fatty acids into the mitochondrial matrix, so they can be broken down through β-oxidation to acetyl CoA to obtain usable energy via the citric acid cycle. In some organisms, such as fungi, the acetate is used in the glyoxylate cycle for gluconeogenesis and formation of carbohydrates. Fatty acids must be activated before being covalently linked to the carnitine molecule to form acylcarnitine for transport. The free fatty acid in the cytosol is first adenylated by reaction with ATP, then attached with a thioester bond to coenzyme A (CoA), with expulsion of AMP. This reaction is catalyzed by the enzyme fatty acyl-CoA synthetase and driven to completion by inorganic pyrophosphatase.

The acyl group on CoA can now be transferred to carnitine and the resulting acylcarnitine transported into the mitochondrial matrix.This occurs via a series of similar steps:

1. Acyl CoA is transferred to the hydroxyl group of carnitine by carnitine acyltransferase I (palmitoyltransferase) located on the outer mitochondrial membrane
2. Acylcarnitine is shuttled inside by a carnitine-acylcarnitine translocase
3. Acylcarnitine is converted to acyl CoA by carnitine acyltransferase II (palmitoyltransferase) located on the inner mitochondrial membrane. The liberated carnitine returns to the cytosol.

Carnitine acyltransferase I and peroxisomal carnitine octanoyl transferase (CROT) undergo allosteric inhibition by malonyl-CoA, an intermediate in fatty acid biosynthesis, to prevent futile cycling between β-oxidation and fatty acid synthesis.

Human genetic disorders, such as primary carnitine deficiency, carnitine palmitoyltransferase I deficiency, carnitine palmitoyltransferase II deficiency and carnitine-acylcarnitine translocase deficiency, affect different steps of this process.

Possible health effects

Carnitine has been proposed as a supplement to treat a variety of health conditions including heart attack, heart failure,angina, narcolepsy,and diabetic neuropathy,but not improving exercise performance, nor wasting syndrome (weight loss). In all of these cases the results are preliminary or proposed, and not part of an established medical treatment.

A note ought to be made about carnitine's purported relationship to seizures. People with epileptic disorders/vulnerability are advised, on product monographs and pharmacy databases, to avoid carnitine and its derivatives as it is claimed to promote epileptic discharges. It now appears that this advice has been misguided. According to a systematic review of epileptics treated with valproic acid, these claims are unsubstantiated both in the scientific litterature and in clinical practice and may have done more harm than good. This is unfortunate as many epileptics actually have decreased levels of carnitine (especially those under valproate treatment) and might need to supplement with this substance in order to avoid troubling side effects (e.g., hepatotoxicity, hyperammonemic encephalopathy). The exact reason for these cautionary notes against carnitine is not known. One possibility is that a well-intended, but ultimately false, disclaimer has propagated uncontrollably throughout pharmacy texts and electronic databases worldwide. Another possibility is that some of the side effects of carnitine (e.g., overstimulation, dizziness, headache, nausea) may mimic, and thus be mistaken for, a mild epileptic fit.