Postprandial endotoxemia may influence the development of type 2 diabetes mellitus: From the CORDIOPREV study
Postprandial endotoxemia may influence the development of type 2 diabetes mellitus: From the CORDIOPREV study
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DOI：
10.1016/j.clnu.2018.03.016
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发表时间：
2019-04-01
影响因子：
6.3
通讯作者：
Lopez-Miranda, Jose
中科院分区：
文献类型：
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作者：
Camargo, Antonio;Jimenez-Lucena, Rosa;Lopez-Miranda, Jose
背景和目标：胰岛素抵抗 (IR) 和 β 细胞功能受损是 2 型糖尿病 (T2DM) 的关键决定因素。肠道吸收细菌成分会激活 Toll 样受体，从而诱发炎症，进而产生 IR。我们评估了内毒素血症在 T2DM 发展过程中促进炎症诱导的胰岛素抵抗 (IR) 的作用，及其作为预测生物标志物的有用性。方法：我们在本研究中纳入了来自 CORDIOPREV 研究的 462 名基线时没有 T2DM 的患者。其中，107 名患者在中位随访 60 个月后根据美国糖尿病协会 (ADA) 诊断标准发展为 T2DM（Incident-DIAB 组），而 355 名患者在此期间没有发展为 T2DM（非 DIAB 组）。 结果：我们观察到基线时 Incident-DIAB 中的脂多糖 (LPS) 水平出现餐后升高 (P < 0.001)，而 LPS 水平则为未在非戴铂中进行修改。与之前描述的 FINRISC 评分相比，基于 LPS 餐后倍数变化的无病生存曲线改善了 T2DM 风险评估（风险比为 2.076，95% CI 1.149-3.750 vs. 1.384，95% CI 0.740 -2.589）。此外，结合餐后LPS倍数变化和FIN-DRISC评分的无病生存曲线显示，风险比为3.835（95% CI 1.323-11.114），与这两个参数的高值相关。结论：我们的结果表明，餐后高内毒素血症先于T2DM的发生。我们的结果还表明 LPS 血浆水平作为 T2DM 发展的生物标志物预测因子的潜在用途。 (C) 2018 Elsevier Ltd 和欧洲临床营养与代谢学会。版权所有。
Background & aims: Insulin resistance (IR) and impaired beta-cell function are key determinants of type 2 diabetes mellitus (T2DM). Intestinal absorption of bacterial components activates the toll-like receptors inducing inflammation, and this in turn IR. We evaluated the role of endotoxemia in promoting inflammation-induced insulin resistance (IR) in the development of T2DM, and its usefulness as predictive biomarker.Methods: We included in this study 462 patients from the CORDIOPREV study without T2DM at baseline. Of these, 107 patients developed T2DM according to the American Diabetes Association (ADA) diagnosis criteria after a median follow-up of 60 months (Incident-DIAB group), whereas 355 patients did not developed it during this period of time (Non-DIAB group).Results: We observed a postprandial increase in lipopolysaccharides (LPS) levels in the Incident-DIAB at baseline (P < 0.001), whereas LPS levels were not modified in the Non-DIAB. Disease-free survival curves based on the LPS postprandial fold change improved T2DM Risk Assessment as compared with the previously described FINDRISC score (hazard ratio of 2.076, 95% CI 1.149-3.750 vs. 1.384, 95% CI 0.740 -2.589). Moreover, disease-free survival curves combining the LPS postprandial fold change and FIN-DRISC score together showed a hazard ratio of 3.835 (95% CI 1.323-11.114), linked to high values of both parameters.Conclusion: Our results suggest that a high postprandial endotoxemia precedes the development of T2DM. Our results also showed the potential use of LPS plasma levels as a biomarker predictor of T2DM development. (C) 2018 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.