Journal article
Isoflavone consumption reduces inflammation through modulation of phenylalanine and lipid metabolism
Metabolomics, Vol.18(11), pp.84-84
10/26/2022
DOI: 10.1007/s11306-022-01944-1
PMCID: PMC10148689
PMID: 36289122
Abstract
Introduction
Phytoestrogens found in soy, fruits, peanuts, and other legumes, have been identified as metabolites capable of providing beneficial effects in multiple pathological conditions due to their ability to mimic endogenous estrogen. Interestingly, the health-promoting effects of some phytoestrogens, such as isoflavones, are dependent on the presence of specific gut bacteria. Specifically, gut bacteria can metabolize isoflavones into equol, which has a higher affinity for endogenous estrogen receptors compared to dietary isoflavones. We have previously shown that patients with multiple sclerosis (MS), a neuroinflammatory disease, lack gut bacteria that are able to metabolize phytoestrogen. Further, we have validated the importance of both isoflavones and phytoestrogen-metabolizing gut bacteria in disease protection utilizing an animal model of MS. Specifically, we have shown that an isoflavone-rich diet can protect from neuroinflammatory diseases, and that protection was dependent on the ability of gut bacteria to metabolize isoflavones into equol. Additionally, mice on a diet with isoflavones showed an anti-inflammatory response compared to the mice on a diet lacking isoflavones. However, it is unknown how isoflavones and/or equol mediates their protective effects, especially their effects on host metabolite levels.
Objectives
In this study, we utilized untargeted metabolomics to identify metabolites found in plasma that were modulated by the presence of dietary isoflavones.
Results
We found that the consumption of isoflavones increased anti-inflammatory monounsaturated fatty acids and beneficial polyunsaturated fatty acids while reducing pro-inflammatory glycerophospholipids, sphingolipids, phenylalanine metabolism, and arachidonic acid derivatives.
Conclusion
Isoflavone consumption alters the systemic metabolic landscape through concurrent increases in monounsaturated fatty acids and beneficial polyunsaturated fatty acids plus reduction in pro-inflammatory metabolites and pathways. This highlights a potential mechanism by which an isoflavone diet may modulate immune-mediated disease.
Details
- Title: Subtitle
- Isoflavone consumption reduces inflammation through modulation of phenylalanine and lipid metabolism
- Creators
- Rachel L. Shrode - University of IowaNicole Cady - University of IowaSamantha N. Jensen - Interdisciplinary Graduate Program in Immunology, University of Iowa, Division of Gastroenterology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell UniversityNicholas Borcherding - Department of Pathology and Immunology, School of Medicine, Washington UniversityAshutosh K. Mangalam - Department of Informatics, University of Iowa, Department of Pathology, Carver College of Medicine, University of Iowa, Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa Institute for Oral Health Research, College of Dentistry, University of Iowa
- Resource Type
- Journal article
- Publication Details
- Metabolomics, Vol.18(11), pp.84-84
- DOI
- 10.1007/s11306-022-01944-1
- PMID
- 36289122
- PMCID
- PMC10148689
- NLM abbreviation
- Metabolomics
- ISSN
- 1573-3882
- eISSN
- 1573-3890
- Publisher
- Springer US
- Grant note
- P. Heppelmann and M. Wacek gift Informatics Fellowship from the University of Iowa 1RO1AI137075 / National Institutes of health/NIAID T32AI007485 / Institutional Training Grant 1RO1AI137075 / Diversity Supplement Award to A.K.M. P30 ES005605 / University of Iowa Environmental Health Sciences Research Center, NIEHS/NIH Carver Trust Pilot Grant 1I01CX002212 / Veteran Affairs Merit Award
- Language
- English
- Date published
- 10/26/2022
- Academic Unit
- Dermatology; Pathology; Iowa Neuroscience Institute
- Record Identifier
- 9984307560302771
Metrics
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