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J. Nutr. First published December 3, 2008; doi:10.3945/jn.108.098269
Journal of Nutrition, doi:10.3945/jn.108.098269
Vol. 139, No. 1, 1-4, January 2009

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© 2009 American Society for Nutrition


Recent Advances in Nutritional Sciences

Saturated Fatty Acid-Mediated Inflammation and Insulin Resistance in Adipose Tissue: Mechanisms of Action and Implications1

Arion Kennedy, Kristina Martinez, Chia-Chi Chuang, Kathy LaPoint and Michael McIntosh*

Department of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27402

This review highlights the inflammatory and insulin-antagonizing effects of saturated fatty acids (SFA), which contribute to the development of metabolic syndrome. Mechanisms responsible for these unhealthy effects of SFA include: 1) accumulation of diacylglycerol and ceramide; 2) activation of nuclear factor-{kappa}B, protein kinase C-{theta}, and mitogen-activated protein kinases, and subsequent induction of inflammatory genes in white adipose tissue, immune cells, and myotubes; 3) decreased PPAR{gamma} coactivator-1 {alpha}/β activation and adiponectin production, which decreases the oxidation of glucose and fatty acids (FA); and 4) recruitment of immune cells like macrophages, neutrophils, and bone marrow-derived dendritic cells to WAT and muscle. Several studies have demonstrated potential health benefits of substituting SFA with unsaturated FA, particularly oleic acid and (n-3) FA. Thus, reducing consumption of foods rich in SFA and increasing consumption of whole grains, fruits, vegetables, lean meats and poultry, fish, low-fat dairy products, and oils containing oleic acid or (n-3) FA is likely to reduce the incidence of metabolic disease.


* To whom correspondence should be addressed. E-mail: mkmcinto{at}uncg.edu.

Published online 3 December 2008.




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