Intestinal alkaline phosphatase prevents metabolic syndrome in mice.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Kaliannan, K; Hamarneh, SR; Economopoulos, KP; Nasrin Alam, S; Moaven, O; Patel, P; Malo, NS; Ray, M; Abtahi, SM; Muhammad, N; Raychowdhury, A; Teshager, A; Mohamed, MMR; Moss, AK; Ahmed, R; Hakimian, S; Narisawa, S; Millán, JL; Hohmann, E; Warren, HS; Bhan, AK; Malo, MS; Hodin, RA

Published Date

  • April 8, 2013

Published In

Volume / Issue

  • 110 / 17

Start / End Page

  • 7003 - 7008

PubMed ID

  • 23569246

Pubmed Central ID

  • 23569246

Electronic International Standard Serial Number (EISSN)

  • 1091-6490

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.1220180110

Language

  • eng