Treatment with Rhodiola crenulata root extract ameliorates insulin resistance in fructose-fed rats by modulating sarcolemmal and intracellular fatty acid translocase/CD36 redistribution in skeletal muscle.
Treatment with Rhodiola crenulata root extract ameliorates insulin resistance in fructose-fed rats by modulating sarcolemmal and intracellular fatty acid translocase/CD36 redistribution in skeletal muscle.
复制标题
用红景天根提取物治疗可通过调节骨骼肌肌膜和细胞内脂肪酸转位酶/CD36 重新分布来改善果糖喂养大鼠的胰岛素抵抗
DOI：
10.1186/s12906-016-1176-z
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发表时间：
2016-07-12
影响因子：
--
通讯作者：
Wang J
中科院分区：
文献类型：
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作者：
Chen T;Yao L;Ke D;Cao W;Zuo G;Zhou L;Jiang J;Yamahara J;Li Y;Wang J
背景红景天被用来治疗虚弱、抑郁、疲劳、工作能力差和心血管疾病，所有这些都可能与胰岛素抵抗有关。为了揭示红景天的作用机制，观察了红景天(Rhodiola Crenulata)对胰岛素抵抗的影响。方法雄性SD大鼠饮用液体果糖18周以上。在过去的5周内，RCR提取物联合给药(每天一次，口服)。用酶标法和/或双抗体夹心法测定血脂和血糖的稳态指标。结果RCR提取物(50 mg/kg)能抑制果糖诱导的高胰岛素血症，抑制稳态模型大鼠胰岛素抵抗指数和脂肪组织胰岛素抵抗指数的升高。此外，这种治疗有恢复葡萄糖与胰岛素和非酯化脂肪酸(NEFA)与胰岛素的比率的趋势。在机制上，RCR抑制果糖引起的血浆NEFA在口服葡萄糖耐量试验(OGTT)中的清除加速，并减少腓肠肌的甘油三酯含量和油红O染色面积。此外，RCR通过促进脂肪酸的摄取，恢复果糖诱导的肌膜过度表达和细胞内脂肪酸转位酶/CD36的较少分布，从而促进胰岛素抵抗的发生。结论RCR通过调节骨骼肌肌膜和细胞内CD36的重新分布，改善果糖喂养大鼠的胰岛素抵抗。我们的发现可能会为更好地理解罗地拉物种的传统用途提供帮助。
BackgroundRhodiola species have been used for asthenia, depression, fatigue, poor work performance and cardiovascular diseases, all of which may be associated with insulin resistance. To disclose the underlying mechanisms of action, the effect of Rhodiola crenulata root (RCR) on insulin resistance was investigated.MethodsMale Sprague-Dawley rats were treated with liquid fructose in their drinking water over 18 weeks. The extract of RCR was co-administered (once daily by oral gavage) during the last 5 weeks. The indexes of lipid and glucose homeostasis were determined enzymatically and/or by ELISA. Gene expression was analyzed by Real-time PCR, Western blot and/or confocal immunofluorescence.ResultsRCR extract (50 mg/kg) suppressed fructose-induced hyperinsulinemia and the increases in the homeostasis model assessment of insulin resistance index and the adipose tissue insulin resistance index in rats. Additionally, this treatment had a trend to restore the ratios of glucose to insulin and non-esterified fatty acids (NEFA) to insulin. Mechanistically, RCR suppressed fructose-induced acceleration of the clearance of plasma NEFA during oral glucose tolerance test (OGTT), and decreased triglyceride content and Oil Red O staining area in the gastrocnemius. Furthermore, RCR restored fructose-induced sarcolemmal overexpression and intracellular less distribution of fatty acid translocase/CD36 that contributes to etiology of insulin resistance by facilitating fatty acid uptake.ConclusionThese results suggest that RCR ameliorates insulin resistance in fructose-fed rats by modulating sarcolemmal and intracellular CD36 redistribution in the skeletal muscle. Our findings may provide a better understanding of the traditional use of Rhodila species.