course=”kwd-title”>Keywords: Adipocytes Fatty acids HAART Mitochondria Type 2 diabetes mellitus Copyright ? The Author(s) 2008 This short article has been cited by other articles in PMC. tissue is usually to prevent leakage of fatty acids into the blood circulation [3]. This mitochondrial activity attenuates the development of ectopic triacylglycerol deposits in the liver and other tissues that would normally contribute to the development of whole body insulin resistance and pancreatic beta cell damage. Mitochondria contribute to efficient confinement of fatty acids within adipocytes by oxidative removal of fatty acids liberated from your triacylglycerol pool by uncoupled beta oxidation. In addition mitochondria may provide glyceroneogenic substrates which contribute to re-esterification of fatty acids. As a net result you will find less fatty acids available to the blood circulation for redistribution to other compartments of the body [3]. A recent study provided supporting evidence for this concept by showing that this mitochondrial DNA copy number in human adipocytes is usually positively CTS-1027 associated with lipogenesis in adipocytes [4].Recently Frayn et al. have argued against this biochemical mechanism [5]. They point out that fatty acid oxidation is not a major pathway in white adipocytes and that oxygen consumption by adipose tissue is usually insufficient to oxidise substantial amounts of fatty acids [6].We fully agree with the point made by the authors that fatty acid oxidation by adipocytes is not a major pathway compared with muscle. However we hold a different view on the quantitative interpretation of these data: in our model there is no need for a high rate of fatty acid oxidation in adipose tissue per time unit as fatty acid redistribution from peripheral tissue to the liver is usually a slow process taking several years. For instance in individuals in whom mitochondrial copy number is usually acutely reduced as result of starting HAART it takes 18-24?months before redistribution of body fat becomes CTS-1027 clinically manifest [7].Therefore the amount of fatty acids that undergoes redistribution per time unit is very small. Thus mitochondria in adipocytes only need to remove a CTS-1027 small amount of fatty acids per time unit CTS-1027 to protect against redistribution of body fat. By using the oxygen consumption data of Frayn et al. as well as others [5 6 or using comparable data from other studies [8 9 one can calculate that oxygen consumption by adipose tissue is sufficient to prevent redistribution of >1.5?kg of fat out of 10?kg of peripheral adipose tissue to the liver within a 3?year period a realistic clinical situation.Therefore in our opinion adipose tissue is able to oxidise substantial amounts of fatty acids over a long period by mitochondrial beta oxidation. This process may over time attenuate ectopic deposition of those fatty acids. Since mitochondria also contribute to formation of glycerol 3-phosphate needed for re-esterification of fatty acids within adipocytes mitochondria in adipocytes have the ability to protect the organism to a certain extent against leakage of fatty acids into the blood circulation and thus redistribution of body fat. As Frayn et al. [5] have pointed out brown adipose tissue is indeed more active in uncoupled oxidative disposal of fatty acids compared with white tissue. Recent evidence also suggests CTS-1027 that brown adipose tissue is present in variable amounts and at multiple sites in humans contrary to earlier reports [10]. This recently recognised situation further enhances the capacity of the adipose compartment to remove fatty acids through uncoupled beta oxidation.In order to understand the mechanism by which Rabbit polyclonal to CD80 mitochondria in adipocytes contribute to the control of body fat distribution during the development of the metabolic syndrome additional studies are needed comprising quantification of fatty acid fluxes in relation to re-esterification and oxidation CTS-1027 in adipose tissue. These studies should include study of adipose tissue from individuals with normal glucose tolerance and from those with developing glucose intolerance. Acknowledgments Duality of interest The authors declare that there is no duality of interest associated with this manuscript. Open Access This short article is usually distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use distribution and reproduction in any medium provided the original writer(s) and supply are credited. Abbreviation active anti-retroviral HAARThighly.