L-Carnitine: Carnitine is is an important essential nutrient, and has been demonstrated to be therapeutic for individuals with narcolepsy.
Carnitine and Narcolepsy. A recent study investigated the contribution of a gene polymorphism found in narcolepsy called CPT1B, which is important in fatty acid oxidation. They discovered that individuals with narcolepsy had very low levels of serum acylcarnitine (see right for the relationship between acylcarnitine and carnitine).
Reduced acylcarnitine means impaired fatty acid oxidation.
In addition, carnintine-deficient mice display phenotypes similar to narcolepsy, included impaired sleep regulation and reduced orexin cell functioning.
Oral supplementation of L-carnitine restores β-oxidation (fatty acid oxidation) and mitochondrial ATP generation from fatty acids.
Carnitine also has marked effects on proper intestinal development and function.
Specifically, it has been shown that carnitine deficiencies lead to severe intestinal and immune phenotypes in mice. In addition to intestinal atrophy, the mice also displayed marked intestinal apoptosis, lymphocyte infiltration and inflammation. There was an increase in CD45-B220(+) lymphocytes [CD45 perturbances have been linked with autoimmune disease], with increased production pro-inflammatory cytokines in immune cells. In addition, carnitine deficiency also causes a down-regulation of TGF-β-induced gene expression [ TGF-β is considered anti-inflammatory]. Carnitine supplementation may reduce intestinal inflammation and improve intestinal (and therefore systemic) health.
Carnitine and the immune system.
Carnitine has also been linked to proper immune cell functioning and improved antioxidant properties of cells. In the intestine, carnitine deficiency causes hyperactivation of CD4+ T cells and enhanced cytokine production. Naive, memory, and regulatory T cells (Tregs; T cells which suppress inflammatory functions of other cells) rely on fatty acid oxidation, while “effector” T cells and pathogenic/inflammatory T cells (as seen in autoimmunity) rely on high rates of glycolysis. Furthermore, inihibiting glycolysis (or improving fatty acid oxidation?) in pathogenic Th17 (autoimmune T cells) will promote Treg development.
Carnitine supplementation can also improve obesity, glucose tolerance and energy expenditure