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Nutritional modulation of metabolic inflammation.
Biochem Soc Trans. 2017 08 15; 45(4):979-985.BS

Abstract

Metabolic inflammation is a very topical area of research, wherein aberrations in metabolic and inflammatory pathways probably contribute to atherosclerosis, insulin resistance (IR) and type 2 diabetes. Metabolic insults arising from obesity promote inflammation, which in turn impedes insulin signalling and reverse cholesterol transport (RCT). Key cells in the process are metabolically activated macrophages, which up-regulate both pro- and anti-inflammatory pathways in response to lipid spillover from adipocytes. Peroxisome proliferator-activated receptors and AMP-activated protein kinase (AMPK) are regulators of cellular homeostasis that influence both inflammatory and metabolic pathways. Dietary fats, such as saturated fatty acids (SFAs), can differentially modulate metabolic inflammation. Palmitic acid, in particular, is a well-characterized nutrient that promotes metabolic inflammation via the NLRP3 (the nod-like receptor containing a pyrin domain) inflammasome, which is partly attributable to AMPK inhibition. Conversely, some unsaturated fatty acids are less potent agonists of metabolic inflammation. For example, monounsaturated fatty acid does not reduce AMPK as potently as SFA and n-3 polyunsaturated fatty acids actively resolve inflammation via resolvins and protectins. Nevertheless, the full extent to which nutritional state modulates metabolic inflammation requires greater clarification.

Authors+Show Affiliations

Nutrigenomics Research Group, Conway Institute of Biomedical and Biomolecular Research, and Institute of Food and Health, University College Dublin, Belfield, Dublin, Ireland.Nutrigenomics Research Group, Conway Institute of Biomedical and Biomolecular Research, and Institute of Food and Health, University College Dublin, Belfield, Dublin, Ireland.Nutrigenomics Research Group, Conway Institute of Biomedical and Biomolecular Research, and Institute of Food and Health, University College Dublin, Belfield, Dublin, Ireland.Nutrigenomics Research Group, Conway Institute of Biomedical and Biomolecular Research, and Institute of Food and Health, University College Dublin, Belfield, Dublin, Ireland. Diabetes Complications Research Centre, Conway Institute of Biomedical and Biomolecular Research, University College Dublin, Belfield, Dublin, Ireland.Nutrigenomics Research Group, Conway Institute of Biomedical and Biomolecular Research, and Institute of Food and Health, University College Dublin, Belfield, Dublin, Ireland helen.roche@ucd.ie.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

28710289

Citation

Kirwan, Anna M., et al. "Nutritional Modulation of Metabolic Inflammation." Biochemical Society Transactions, vol. 45, no. 4, 2017, pp. 979-985.
Kirwan AM, Lenighan YM, O'Reilly ME, et al. Nutritional modulation of metabolic inflammation. Biochem Soc Trans. 2017;45(4):979-985.
Kirwan, A. M., Lenighan, Y. M., O'Reilly, M. E., McGillicuddy, F. C., & Roche, H. M. (2017). Nutritional modulation of metabolic inflammation. Biochemical Society Transactions, 45(4), 979-985. https://doi.org/10.1042/BST20160465
Kirwan AM, et al. Nutritional Modulation of Metabolic Inflammation. Biochem Soc Trans. 2017 08 15;45(4):979-985. PubMed PMID: 28710289.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nutritional modulation of metabolic inflammation. AU - Kirwan,Anna M, AU - Lenighan,Yvonne M, AU - O'Reilly,Marcella E, AU - McGillicuddy,Fiona C, AU - Roche,Helen M, Y1 - 2017/07/14/ PY - 2017/03/13/received PY - 2017/05/11/revised PY - 2017/05/16/accepted PY - 2017/7/16/pubmed PY - 2017/12/30/medline PY - 2017/7/16/entrez KW - fatty acids KW - inflammation KW - insulin resistance KW - metabolism KW - nutrients KW - reverse cholesterol transport SP - 979 EP - 985 JF - Biochemical Society transactions JO - Biochem Soc Trans VL - 45 IS - 4 N2 - Metabolic inflammation is a very topical area of research, wherein aberrations in metabolic and inflammatory pathways probably contribute to atherosclerosis, insulin resistance (IR) and type 2 diabetes. Metabolic insults arising from obesity promote inflammation, which in turn impedes insulin signalling and reverse cholesterol transport (RCT). Key cells in the process are metabolically activated macrophages, which up-regulate both pro- and anti-inflammatory pathways in response to lipid spillover from adipocytes. Peroxisome proliferator-activated receptors and AMP-activated protein kinase (AMPK) are regulators of cellular homeostasis that influence both inflammatory and metabolic pathways. Dietary fats, such as saturated fatty acids (SFAs), can differentially modulate metabolic inflammation. Palmitic acid, in particular, is a well-characterized nutrient that promotes metabolic inflammation via the NLRP3 (the nod-like receptor containing a pyrin domain) inflammasome, which is partly attributable to AMPK inhibition. Conversely, some unsaturated fatty acids are less potent agonists of metabolic inflammation. For example, monounsaturated fatty acid does not reduce AMPK as potently as SFA and n-3 polyunsaturated fatty acids actively resolve inflammation via resolvins and protectins. Nevertheless, the full extent to which nutritional state modulates metabolic inflammation requires greater clarification. SN - 1470-8752 UR - https://www.unboundmedicine.com/medline/citation/28710289/Nutritional_modulation_of_metabolic_inflammation_ L2 - https://portlandpress.com/biochemsoctrans/article-lookup/doi/10.1042/BST20160465 DB - PRIME DP - Unbound Medicine ER -