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首页> 外文期刊>American Journal of Physiology >CB1R antagonist increases hepatic insulin clearance in fat-fed dogs likely via upregulation of liver adiponectin receptors
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CB1R antagonist increases hepatic insulin clearance in fat-fed dogs likely via upregulation of liver adiponectin receptors

机译：CB1R拮抗剂可能通过肝脏脂联素受体的上调，增加脂肪喂养犬的肝胰岛素清除

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The improvement of hepatic insulin sensitivity by the cannabinoid receptor 1 (CB1R) antagonist rimonabant (RIM) has been recently been reported to be due to upregulation of adiponectin. Several studies demonstrated that improvement in insulin clearance accompanies the enhancement of hepatic insulin sensitivity. However, the effects of RIM on hepatic insulin clearance (HIC) have not been fully explored. The aim of this study was to explore the molecular mechanism(s) by which RIM affects HIC, specifically to determine whether upregulation of liver adiponectin receptors (ADRs) and other key genes regulated by adiponectin mediate the effects. To induce insulin resistance in skeletal muscle and liver, dogs were fed a hypercaloric high-fat diet (HFD) for 6 wk. Thereafter, while still maintained on a HFD, animals received RIM (HFD+RIM; n = 11) or placebo (HFD+PL; n = 9) for an additional 16 wk. HIC, calculated as the metabolic clearance rate (MCR), was estimated from the euglycemic-hyperinsulinemic clamp. The HFD+PL group showed a decrease in MCR; in contrast, the HFD+RIM group increased MCR. Consistently, the expression of genes involved in HIC, CEACAM-1 and IDE, as well as gene expression of liver ADRs, were increased in the HFD+RIM group, but not in the HFD+PL group. We also found a positive correlation between CEACAM-1 and the insulin-degrading enzyme IDE with ADRs. Interestingly, expression of liver genes regulated by adiponectin and involved in lipid oxidation were increased in the HFD+RIM group. We conclude that in fat-fed dogs RIM enhances HIC, which appears to be linked to an upregulation of the adiponectin pathway.
机译：最近据报道，大麻素受体1（CB1R）拮抗剂乙孢菌素（RIM）的肝胰岛素敏感性的提高是由于脂联素的上调。几项研究表明，胰岛素清除的改善伴随着肝胰岛素敏感性的增强。然而，RIM对肝胰岛素清除（HIC）的影响尚未得到充分探索。本研究的目的是探讨轮辋影响HIC的分子机制，特别是确定肝脏脂联素受体（ADRS）的上调和由脂联素调节的其他关键基因介导效果。为了诱导骨骼肌和肝脏中的胰岛素抵抗，犬喂养过高脂肪饮食（HFD）6周。此后，仍然保持在HFD上，动物接收边缘（HFD + RIM; n = 11）或安慰剂（HFD + PL; n = 9），另外16周。作为代谢清除率（MCR）计算的HIC，估计来自外酰血糖性高胰岛素血症纤维素含量。 HFD + PL组显示MCR减少;相反，HFD + RIM组增加了MCR。始终如一地，在HIC + RIM基团中增加了HIC，CeAcam-1和IDE中参与的基因，以及肝脏ADR的基因表达，但不在HFD + PL组中增加。我们还发现CEACAM-1与胰岛素降解酶IDE之间的正相关性。有趣的是，HFD + RIM基团中增加了脂联素调节并参与脂氧化的肝脏基因的表达。我们得出结论，在脂肪喂养的狗中，RIM增强了HIC，其似乎与脂联素途径的上调有关。

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