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首页> 外文期刊>Life sciences >Pioglitazone upregulates adiponectin receptor 2 in 3T3-L1 adipocytes.
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Pioglitazone upregulates adiponectin receptor 2 in 3T3-L1 adipocytes.

机译：吡格列酮上调3T3-L1脂肪细胞中的脂联素受体2。

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AIMS: Pioglitazone, a full peroxisome proliferator-activated receptor (PPAR)-gamma agonist, improves insulin sensitivity by increasing circulating adiponectin levels. However, the molecular mechanisms by which pioglitazone induces insulin sensitization are not fully understood. In this study, we investigated whether pioglitazone improves insulin resistance via upregulation of either 2 distinct receptors for adiponectin (AdipoR1 or AdipoR2) expression in 3T3-L1 adipocytes. MAIN METHODS: Glucose uptake was evaluated by 2-[(3)H] deoxy-glucose uptake assay in 3T3-L1 adipocytes with pioglitazone treatment. AdipoR1 and AdipoR2 mRNA expressions were analyzed by qRT-PCR. KEY FINDINGS: We first confirmed that pioglitazone significantly increased insulin-induced 2-deoxyglucose (2-DOG) uptake in 3T3-L1 adipocytes. Next, we investigated the mRNA expression and regulation of AdipoR1 and AdipoR2 after treatment with pioglitazone. Interestingly, pioglitazone significantly induced AdipoR2 expression but it did not affect AdipoR1 expression. In addition, adenovirus-mediated PPARgamma expression significantly enhanced the effects of pioglitazone on insulin-stimulated 2-DOG uptake and AdipoR2 expression in 3T3-L1 adipocytes. These data suggest that pioglitazone enhances adiponectin's autocrine and paracrine actions in 3T3-L1 adipocytes via upregulation of PPARgamma-mediated AdipoR2 expression. Furthermore, we found that pioglitazone significantly increased AMP-activated protein kinase (AMPK) phosphorylation in insulin-stimulated 3T3-L1 adipocytes, but it did not lead to the phosphorylation of IRS-1, Akt, or protein kinase Clambda/zeta. SIGNIFICANCE: Our results suggest that pioglitazone increases insulin sensitivity, at least partly, by PPARgamma-AdipoR2-mediated AMPK phosphorylation in 3T3-L1 adipocytes. In conclusion, the upregulation of AdipoR2 expression may be one of the mechanisms by which pioglitazone improves insulin resistance in 3T3-L1 adipocytes.
机译：目的：吡格列酮是一种完整的过氧化物酶体增殖物激活受体（PPAR）-γ激动剂，可通过增加循环脂联素水平来提高胰岛素敏感性。但是，吡格列酮诱导胰岛素致敏的分子机制尚未完全了解。在这项研究中，我们调查了吡格列酮是否通过上调3T3-L1脂肪细胞中脂联素的2个不同受体（AdipoR1或AdipoR2）的表达来提高胰岛素抵抗。主要方法：通过吡格列酮处理的3T3-L1脂肪细胞中的2-[（（3）H]脱氧葡萄糖摄取试验）评估了葡萄糖摄取。通过qRT-PCR分析AdipoR1和AdipoR2 mRNA的表达。主要发现：我们首先证实吡格列酮显着增加了3T3-L1脂肪细胞中胰岛素诱导的2-脱氧葡萄糖（2-DOG）摄取。接下来，我们研究了吡格列酮治疗后AdipoR1和AdipoR2的mRNA表达和调控。有趣的是，吡格列酮显着诱导AdipoR2表达，但不影响AdipoR1表达。此外，腺病毒介导的PPARγ表达显着增强了吡格列酮对3T3-L1脂肪细胞中胰岛素刺激的2-DOG摄取和AdipoR2表达的影响。这些数据表明，吡格列酮可通过上调PPARγ介导的AdipoR2表达来增强3T3-L1脂肪细胞中脂联素的自分泌和旁分泌作用。此外，我们发现吡格列酮显着增加了胰岛素刺激的3T3-L1脂肪细胞中AMP激活的蛋白激酶（AMPK）的磷酸化，但并未导致IRS-1，Akt或蛋白激酶Clambda / zeta的磷酸化。意义：我们的结果表明，吡格列酮至少部分地通过3T3-L1脂肪细胞中PPARgamma-AdipoR2介导的AMPK磷酸化提高胰岛素敏感性。总之，AdipoR2表达的上调可能是吡格列酮改善3T3-L1脂肪细胞胰岛素抵抗的机制之一。

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