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Metabolic inflexibility of white and brown adipose tissues in abnormal fatty acid partitioning of type 2 diabetes

Abstract

Type 2 diabetes (T2D) is characterized by a general dysregulation of postprandial energy substrate partitioning. Although classically described in regard to glucose metabolism, it is now evident that metabolic inflexibility of plasma lipid fluxes is also present in T2D. The organ that is most importantly involved in the latter metabolic defect is the white adipose tissue (WAT). Both catecholamine-induced nonesterified fatty acid mobilization and insulin-stimulated storage of meal fatty acids are impaired in many WAT depots of insulin-resistant individuals. Novel molecular imaging techniques now demonstrate that these defects are linked to increased dietary fatty acid fluxes toward lean organs and myocardial dysfunction in humans. Recent findings also demonstrate functional abnormalities of brown adipose tissues in T2D, thus suggesting that a generalized adipose tissue dysregulation of energy storage and dissipation may be at play in the development of lean tissue energy overload and lipotoxicity.

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Acknowledgements

SML is the recipient of a Canadian Diabetes Association doctoral studentship. ACC is the recipient of the CIHR-GSK Chair in Diabetes.

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Correspondence to A C Carpentier.

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This article was published as part of a supplement funded with an unrestricted educational contribution from Desjardins Sécurité Financière.

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Grenier-Larouche, T., Labbé, S., Noll, C. et al. Metabolic inflexibility of white and brown adipose tissues in abnormal fatty acid partitioning of type 2 diabetes. Int J Obes Supp 2 (Suppl 2), S37–S42 (2012). https://doi.org/10.1038/ijosup.2012.21

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