Journal article
The relationship between vitamin C status, the gut-liver axis, and metabolic syndrome
Redox biology, Vol.21, pp.101091-101091
02/2019
DOI: 10.1016/j.redox.2018.101091
PMCID: PMC6327911
PMID: 30640128
Abstract
Metabolic syndrome (MetS) is a constellation of cardiometabolic risk factors, which together predict increased risk of more serious chronic diseases. We propose that one consequence of dietary overnutrition is increased abundance of Gram-negative bacteria in the gut that cause increased inflammation, impaired gut function, and endotoxemia that further dysregulate the already compromised antioxidant vitamin status in MetS. This discussion is timely because "healthy" individuals are no longer the societal norm and specialized dietary requirements are needed for the growing prevalence of MetS. Further, these lines of evidence provide the foundational basis for investigation that poor vitamin C status promotes endotoxemia, leading to metabolic dysfunction that impairs vitamin E trafficking through a mechanism involving the gut-liver axis. This report will establish a critical need for translational research aimed at validating therapeutic approaches to manage endotoxemia-an early, but inflammation-inducing phenomenon, which not only occurs in MetS, but is also prognostic of more advanced metabolic disorders including type 2 diabetes mellitus, as well as the increasing severity of nonalcoholic fatty liver diseases.
Details
- Title: Subtitle
- The relationship between vitamin C status, the gut-liver axis, and metabolic syndrome
- Creators
- Maret G Traber - Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USAGarry R Buettner - Free Radical & Radiation Biology Program, The University of Iowa, Iowa City, IA 52242, USARichard S Bruno - Human Nutrition Program, The Ohio State University, Columbus, OH 43210, USA. Electronic address: bruno.27@osu.edu
- Resource Type
- Journal article
- Publication Details
- Redox biology, Vol.21, pp.101091-101091
- DOI
- 10.1016/j.redox.2018.101091
- PMID
- 30640128
- PMCID
- PMC6327911
- NLM abbreviation
- Redox Biol
- ISSN
- 2213-2317
- eISSN
- 2213-2317
- Publisher
- Netherlands
- Grant note
- P30 ES005605 / NIEHS NIH HHS R01 DK081761 / NIDDK NIH HHS UL1 TR001070 / NCATS NIH HHS R01 CA169046 / NCI NIH HHS
- Language
- English
- Date published
- 02/2019
- Academic Unit
- Radiation Oncology
- Record Identifier
- 9984047753302771
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