Background: Although carnitine is best known for its role in the import of long-chain fatty acids (acyl groups) into the mitochondrial matrix for subsequent β-oxidation, carnitine is also necessary for the efflux of acyl groups out of the mitochondria. Since intracellular accumulation of acyl-CoA derivatives has been implicated in the development of insulin resistance, carnitine supplementation has gained attention as a tool for the treatment of insulin resistance. More recent studies even point toward a causative role for carnitine insufficiency in developing insulin resistance during states of chronic metabolic stress, such as obesity, which can be reversed by carnitine supplementation.
Methods: The present review provides an overview about data from both animal and human studies reporting effects of either carnitine supplementation or carnitine deficiency on parameters of glucose homeostasis and insulin sensitivity in order to establish the less well-recognized role of carnitine in regulating glucose homeostasis.
Results: Carnitine supplementation studies in both humans and animals demonstrate an improvement of glucose tolerance, in particular during insulin-resistant states. In contrast, less consistent results are available from animal studies investigating the association between carnitine deficiency and glucose intolerance. The majority of studies dealing with this question could either find no association or even reported that carnitine deficiency lowers blood glucose and improves insulin sensitivity.
Conclusions: In view of the abovementioned beneficial effect of carnitine supplementation on glucose tolerance during insulin-resistant states, carnitine supplementation might be an effective tool for improvement of glucose utilization in obese type 2 diabetic patients. However, further studies are necessary to explain the conflicting observations from studies dealing with carnitine deficiency.