Abstract
Obesity is frequently associated with the development of type 2 diabetes which is firstly characterized by a defect in the response of key metabolic tissues to insulin (insulin resistance). The imbalance in fatty composition of the diet, a low-grade inflammatory state have been described to be involved in the initiation or the amplification of the molecular events involved in this process. The concept of a specific nutritional intervention has emerged as a promising tool against metabolic disorders associated with obesity. In this context, many investigations were conducted to evaluate the potential beneficial impacts of n−3 polyunsaturated fatty acids (n−3 PUFA). The aim of the present review was to summarize the current knowledge about the role of docosahexanoic acid (DHA, 22:6n−3) and eicosapentanoic acid (EPA, 20:5n−3) on key metabolic organs. Only studies aiming to understand the mechanism of actions were selected. The analysis of randomized clinical trial about n−3 PUFA was not considered here. The effects of n−3 PUFA were analyzed in the adipose tissue, the liver, skeletal muscle and the pancreas in the context of obesity and lipid oversupply. Furthermore, in line with recent findings about the role of the modulation of gut microbiota in obesity-related disorders, we summarized the recent findings about the possible link between n−3 PUFA and change in microbiota composition.
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We gratefully acknowledge financial support from Sofiproteol for the Ph D thesis of A. Pinel and our research.
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The authors disclose no relevant conflict of interest. The authors are grateful to the Sofiproteol company who provided fund to the authors for conducting researches during the last years. The company did not provide the fatty acids used in our experiments. The authors declare that they were completely free to write and to elaborate the content of the present review.
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Pinel, A., Morio-Liondore, B. & Capel, F. n−3 polyunsaturated fatty acids modulate metabolism of insulin-sensitive tissues: implication for the prevention of type 2 diabetes. J Physiol Biochem 70, 647–658 (2014). https://doi.org/10.1007/s13105-013-0303-2
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DOI: https://doi.org/10.1007/s13105-013-0303-2