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一种新型有机矿物复合物可预防高脂饮食诱导的青年雄性 Sprague-Dawley 大鼠高血糖、内毒素血症、肝损伤和内皮功能障碍。

A novel organic mineral complex prevented high fat diet-induced hyperglycemia, endotoxemia, liver injury and endothelial dysfunction in young male Sprague-Dawley rats.

机构信息

School of Life Sciences, Arizona State University, Tempe, Arizona, United States of America.

Isagenix International, LLC, Gilbert, Arizona, United States of America.

出版信息

PLoS One. 2019 Aug 26;14(8):e0221392. doi: 10.1371/journal.pone.0221392. eCollection 2019.

DOI:10.1371/journal.pone.0221392
PMID:31449541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6709910/
Abstract

The prevalence of metabolic syndrome (MetSyn) has risen 35% since 2012 and over two-thirds of Americans exhibit features characterizing this condition (obesity, dyslipidemia, hyperglycemia, insulin resistance and/or endothelial dysfunction). The aim of this study was to evaluate the effects of a novel dietary supplemental organic mineral complex (OMC) on these risk factors in a rodent model of MetSyn. Six-week old male Sprague-Dawley rats were fed either standard chow or a high-fat diet (HFD) composed of 60% kcal from fat for 10 weeks. Rats were also treated with OMC in their drinking water at either 0 mg/mL (control), 0.6 mg/mL, or 3.0 mg/mL. The HFD-treated rats exhibited significantly increased body mass (p<0.05), epididymal fat pad mass (p<0.001), waist circumference (p = 0.010), in addition to elevations in plasma endotoxins (p<0.001), ALT activity (p<0.001), fasting serum glucose (p = 0.025) and insulin concentrations (p = 0.009). OMC did not affect body weight or adiposity induced by the HFD. At the higher dose OMC significantly blunted HFD-induced hyperglycemia (p = 0.021), whereas both low and high doses of OMC prevented HFD-induced endotoxemia (p = 0.002 and <0.001, respectively) and hepatocyte injury (ALT activity, p<0.01). Despite evidence of oxidative stress (elevated urinary H2O2 p = 0.032) in HFD-fed rats, OMC exhibited no demonstrable antioxidative effect. Consistent with prior studies, mesenteric arteries from HFD rats had more uncoupled eNOS (p = 0.006) and iNOS protein expression (p = 0.027) in addition to impaired endothelium-dependent vasodilation that was abrogated by the high dose of OMC (p<0.05). This effect of OMC may be attributed to the high nitrate content of the supplement. These findings suggest that the OMC supplement, particularly at the higher dose, ameliorated several risk factors associated with MetSyn via a non-antioxidant-dependent mechanism.

摘要

代谢综合征(MetSyn)的患病率自 2012 年以来上升了 35%,超过三分之二的美国人表现出这种病症的特征(肥胖、血脂异常、高血糖、胰岛素抵抗和/或内皮功能障碍)。本研究旨在评估一种新型膳食补充有机矿物质复合物(OMC)对代谢综合征啮齿动物模型中这些风险因素的影响。6 周龄雄性 Sprague-Dawley 大鼠喂食标准饲料或高脂肪饮食(HFD),其中 60%的热量来自脂肪,持续 10 周。大鼠还在饮用水中接受 OMC 治疗,剂量分别为 0mg/mL(对照)、0.6mg/mL 或 3.0mg/mL。HFD 处理的大鼠表现出显著增加的体重(p<0.05)、附睾脂肪垫质量(p<0.001)、腰围(p=0.010),以及血浆内毒素(p<0.001)、ALT 活性(p<0.001)、空腹血清葡萄糖(p=0.025)和胰岛素浓度(p=0.009)的升高。OMC 对 HFD 诱导的体重或肥胖没有影响。在较高剂量下,OMC 显著减轻 HFD 诱导的高血糖(p=0.021),而低剂量和高剂量的 OMC 分别预防 HFD 诱导的内毒素血症(p=0.002 和 <0.001)和肝细胞损伤(ALT 活性,p<0.01)。尽管 HFD 喂养的大鼠尿液中存在氧化应激的证据(H2O2 升高,p=0.032),但 OMC 没有表现出明显的抗氧化作用。与先前的研究一致,HFD 大鼠的肠系膜动脉中 eNOS(p=0.006)和 iNOS 蛋白表达(p=0.027)的解偶联增加,内皮依赖性血管舒张受损,而高剂量的 OMC 可消除这种作用(p<0.05)。OMC 的这种作用可能归因于补充剂中的高硝酸盐含量。这些发现表明,OMC 补充剂,特别是高剂量,通过非抗氧化依赖机制改善了与 MetSyn 相关的几种风险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69e/6709910/170c53b54089/pone.0221392.g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69e/6709910/33601287c7bb/pone.0221392.g002.jpg
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