Intestinal alkaline phosphatase prevents metabolic syndrome in mice
Intestinal alkaline phosphatase prevents metabolic syndrome in mice
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DOI：
10.1073/pnas.1220180110
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发表时间：
2013-04-23
影响因子：
11.1
通讯作者：
Hodin, Richard A.
中科院分区：
文献类型：
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作者：
Kaliannan, Kanakaraju;Hamarneh, Sulaiman R.;Hodin, Richard A.
代谢综合征包括一系列相关的疾病，包括肥胖、糖耐量低减、胰岛素抵抗、血脂异常和脂肪肝。最近，肠源性慢性内毒素血症被认为是触发低度炎症的主要介质，而低度炎症是导致代谢综合征发生的原因。在目前的研究中，我们研究了小肠刷状缘酶，肠道碱性磷酸酶(IAP)在预防高脂饮食诱导的小鼠代谢综合征中的作用。我们发现，内源性和口服补充IAP都能抑制饮食脂肪对内毒素(脂多糖)的吸收，口服IAP既能预防代谢综合征，也能逆转代谢综合征。此外，补充IAP改善了喂食标准低脂饮食的小鼠的血脂状况。这些结果指出了一种针对高危人类代谢综合征的潜在独特疗法。
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.