Intestinal alkaline phosphatase prevents metabolic syndrome in mice

Dyslipidemia
DOI: 10.1073/pnas.1220180110 Publication Date: 2013-04-09T01:18:31Z
ABSTRACT
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 primary mediator for triggering the low-grade inflammation responsible development metabolic syndrome. In present study we examined role small intestinal brush-border enzyme, alkaline phosphatase (IAP), in preventing high-fat-diet-induced mice. We found both endogenous orally supplemented IAP inhibits absorption endotoxin (lipopolysaccharides) occurs with dietary fat, oral supplementation prevents well reverses Furthermore, improves lipid profile mice fed standard, low-fat chow diet. These results point to potentially unique therapy against at-risk humans.
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