Correction: PID1 alters the antilipolytic action of insulin and increases lipolysis via inhibition of AKT/PKA pathway activation
Correction: PID1 alters the antilipolytic action of insulin and increases lipolysis via inhibition of AKT/PKA pathway activation
复制标题
修正：PID1 改变胰岛素的抗脂解作用，并通过抑制 AKT/PKA 通路激活来增加脂解作用
DOI：
10.1371/journal.pone.0214606
复制
发表时间：
2019-06
期刊：
影响因子：
3.7
通讯作者：
Yanfeng Xiao
中科院分区：
文献类型：
--
作者：
Chunyan Yin;Wei hua Liu;Yuesheng Liu;Li Wang;Yanfeng Xiao
目的：本研究的目的是研究含1磷酸酪氨酸相互作用结构域(PID1)对胰岛素诱导的AKT(蛋白激酶B)/蛋白激酶A(PKA)/激素敏感脂肪酶(HSL)途径和脂肪分解的影响。检测两组胰岛素、甘油、游离脂肪酸(FFAs)和PID1基因表达水平。此外，我们还研究了PID1在3T3-L1细胞AKT/PKA/HSL级联和脂解过程中的调节作用。结果：HFD大鼠脂肪组织中PID1的表达升高，与胰岛素水平和脂解作用呈正相关。在3T3-L1脂肪细胞中，我们发现胰岛素的抗脂作用是由AKT介导的，而AKT的磷酸化可促进PDE3B的表达，使PKA和HSL去磷酸化，并抑制甘油的释放。在3T3-L1细胞中，PID1过表达及1μM异丙肾上腺素和100 nM胰岛素处理24 h后，细胞内甘油释放量增加，AKT磷酸化、PDE3B表达和PKA/HSL的磷酸化均受到明显抑制。相反，抑制PID1和上述试剂治疗可抑制脂肪分解并激活AKT的磷酸化，从而导致PKA和HSL的去磷酸化。结论：我们的研究结果表明，脂肪组织中的PID1通过改变胰岛素的抗脂作用而增加脂肪分解。这表明PID1可能是改善脂肪细胞脂解从而提高胰岛素敏感性的新的治疗靶点。
Purpose.The aim of this study was to investigate the effect of phosphotyrosine interaction domain.containing 1 (PID1) on the insulin-induced activation of the AKT (protein kinase B)/protein.kinase A (PKA)/hormone-sensitive lipase (HSL) pathway and lipolysis..Methods.Sprague–Dawley rats were fed either chow or a high-fat diet (HFD). The levels of insulin,.glycerol, free fatty acids (FFAs) and PID1 mRNA expression were measured in the 2.groups. Furthermore, we examined the role of PID1 in the regulation of the AKT/PKA/HSL.cascade and lipolysis in the 3T3-L1 cell line..Results.Adipose tissue from HFD rats exhibited elevated PID1 expression, which showed a positive.correlation with insulin levels and lipolysis. In 3T3-L1 adipocytes, we found that the antilipolytic.effect of insulin is mediated by AKT and that phosphorylated AKT results in the promotion.of PDE3B expression, the dephosphorylation of PKA and HSL and the suppression of.glycerol release. However, overexpression of PID1 and treatment with 1 μM isoproterenol.and 100 nM insulin for 24 h resulted in an increased release of glycerol and a noticeable inhibition.of AKT phosphorylation, PDE3B expression and the phosphorylation of PKA/HSL in.3T3-L1 cells. In contrast, knockdown of PID1 and treatment with the above reagents inhibited.lipolysis and activated the phosphorylation of AKT, which resulted in the dephosphorylation.of PKA and HSL..Conclusions.Our findings indicate that PID1 in adipose tissue increases lipolysis by altering the antilipolytic.action of insulin. This suggests that PID1 may represent a new therapeutic target to ameliorate.adipocyte lipolysis and hence improve insulin sensitivity.
修正：PID1 改变胰岛素的抗脂解作用，并通过抑制 AKT/PKA 通路激活来增加脂解作用
影响因子：
3.7
作者：
Chunyan Yin;Wei hua Liu;Yuesheng Liu;Li Wang;Yanfeng Xiao
通讯作者：
Yanfeng Xiao