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Intestinal alkaline phosphatase prevents metabolic syndrome in mice.
Metabolic syndrome comprises a cluster of related disorders that includes obesity, glucose intolerance, insulin resistance, dyslipidemia, and fatty liver. Recently, gut-derived chronic endotoxemia has been identified as a primary mediator for triggering the low-grade inflammation responsible for the development of metabolic syndrome. In the present study we examined the role of the small intestinal brush-border enzyme, intestinal alkaline phosphatase (IAP), in preventing a high-fat-diet-induced metabolic syndrome in mice. We found that both endogenous and orally supplemented IAP inhibits absorption of endotoxin (lipopolysaccharides) that occurs with dietary fat, and oral IAP supplementation prevents as well as reverses metabolic syndrome. Furthermore, IAP supplementation improves the lipid profile in mice fed a standard, low-fat chow diet. These results point to a potentially unique therapy against metabolic syndrome in at-risk humans.
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Related Subject Headings
- Triglycerides
- Real-Time Polymerase Chain Reaction
- Microvilli
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Metabolic Syndrome
- Liver
- Lipopolysaccharides
- DNA Primers
Citation
![Journal cover image](https://secure.syndetics.com/index.aspx?isbn=/lc.gif&issn=1091-6490&client=dukeuniv)
Published In
DOI
EISSN
ISSN
Publication Date
Volume
Issue
Start / End Page
Related Subject Headings
- Triglycerides
- Real-Time Polymerase Chain Reaction
- Microvilli
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Metabolic Syndrome
- Liver
- Lipopolysaccharides
- DNA Primers