Inability to utilize Carnitine due to aging or obesity leads to elevated blood sugar and the inability to create energy

L-Carnitine is a very important amino acid. It carries the fatty acids derived from food into our cells many power-plants where these fats are used as fuel to create energy; the power plants are called mitochondria. Creating this energy makes organs and systems run efficiently. After dropping off the fatty acids that are used for fuel the Carnitine picks up waste material and carries it out of the cell.

Scientists at Duke University note that recent evidence indicates that L- Carnitine requirements increase under conditions of sustained metabolic stress. Accordingly, they hypothesized that lacking sufficient Carnitine in the obese might contribute to mitochondrial dysfunction and the impairment in utilization of insulin leading to elevated blood sugar. Consistent with this prediction the decline of Carnitine in the entire body was identified as a common feature of insulin resistant states such as advanced age, genetic diabetes and diet-induced obesity.

In rodents fed a lifelong high fat diet, compromised Carnitine status corresponded with increased skeletal muscle accumulation of acylcarnitine esters (waste product) and diminished function of genes in the liver that create Carnitine. A diminished Carnitine reserve in muscle of obese rats was accompanied by marked disturbance in fuel metabolism, including low rates of complete fatty acid oxidation (the fatty acids were not used efficiently for fuel). These mitochondrial abnormalities were reversed by eight weeks of oral Carnitine supplementation, in concert with increased tissue efflux and urinary excretion of Acetyl-Carnitine and improvement of whole body glucose tolerance. Acetyl-Carnitine is produced by the mitochondrial matrix enzyme, Carnitine acetyltransferase (CrAT). A role for this enzyme in combating glucose intolerance was further supported by the finding that CrAT overexpression in primary human skeletal myocytes increased glucose uptake and reduced fatty diet induced suppression of glucose oxidation. These results implicate Carnitine insufficiency and reduced CrAT activity as reversible components of metabolic syndrome. The study is published in the June 24, 2009 issue of the Journal of Biological Chemistry.