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首页> 外文期刊>American Journal of Physiology >Acute effects of wortmannin on insulin's hemodynamic and metabolic actions in vivo.
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Acute effects of wortmannin on insulin's hemodynamic and metabolic actions in vivo.

机译：渥曼青霉素对体内胰岛素的血液动力学和代谢作用的急性作用。

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Wortmannin, an inhibitor of phosphatidylinositol 3-kinase, was systemically infused during a hyperinsulinemic euglycemic clamp to investigate its effects in vivo. Rats were infused under anesthesia with saline, 10 or 20 mU.min-1.kg-1 insulin, wortmannin (1 microg.min-1.kg-1)+saline, or wortmannin+insulin (10 mU.min-1.kg-1); wortmannin was present for 1 h before and throughout the 2-h clamp. Femoral blood flow (FBF), glucose infusion rate to maintain euglycemia (GIR), glucose appearance (Ra), glucose disappearance (Rd), capillary recruitment by 1-methylxanthine metabolism (MXD), hindleg glucose uptake (HLGU), liver, muscle, and aorta Akt phosphorylation (P-Akt/Akt), and plasma insulin concentrations were determined. Plasma insulin increased from 410+/-49 to 1,680+/-430 and 5,060+/-230 pM with 10 and 20 mU.min-1.kg-1 insulin, respectively. Insulin (10 and 20 mU.min-1.kg-1) increased FBF, MXD, GIR, Rd, and HLGU as well as liver, muscle, and aorta P-Akt/Akt and decreased Ra (all P<0.05). Wortmannin alone increased plasma insulin to 5,450+/-770 pM and increased Ra, Rd, HLGU, and muscle P-Akt/Akt without effect on blood glucose, FBF, MXD liver, or aorta P-Akt/Akt. Wortmannin blocked FBF, MXD, and liver P-Akt/Akt increases from 10 mU.min-1.kg-1 insulin. Comparison of wortmannin+10 mU.min-1.kg-1 insulin and 20 mU.min-1.kg-1 insulin alone (both at approximately 5,000 pM PI) showed that wortmannin fully blocked the changes in FBF and Ra and partly those of GIR, Ra, Rd, HLGU, and muscle P-AKT/Akt. In summary, wortmannin in vivo increases plasma insulin and fully inhibits insulin-mediated effects in liver and aorta and partially those of muscle, where the latter may result from inhibition of insulin-mediated increases in blood flow and capillary recruitment.
机译：Wortmannin是磷脂酰肌醇3激酶的抑制剂，在高胰岛素正常血糖钳夹期间被全身性输注，以研究其在体内的作用。在麻醉下向大鼠输注盐水，10或20 mU.min-1.kg-1胰岛素，渥曼青霉素（1 microg.min-1.kg-1）+盐水或渥曼青霉素+胰岛素（10 mU.min-1）。公斤-1）;渥曼青霉素在2小时钳夹之前和整个过程中存在1小时。股血流量（FBF），维持正常血糖的葡萄糖输注速率（GIR），葡萄糖外观（Ra），葡萄糖消失（Rd），1-甲基黄嘌呤代谢引起的毛细血管补充（MXD），后腿葡萄糖摄取（HLGU），肝脏，肌肉测定主动脉Akt磷酸化（P-Akt / Akt）和血浆胰岛素浓度。使用10和20 mU.min-1.kg-1胰岛素时，血浆胰岛素分别从410 +/- 49增至1,680 +/- 430和5,060 +/- 230 pM。胰岛素（10和20 mU.min-1.kg-1）增加FBF，MXD，GIR，Rd和HLGU以及肝，肌肉和主动脉P-Akt / Akt并降低Ra（所有P <0.05）。单独使用Wortmannin可使血浆胰岛素增加至5,450 +/- 770 pM，并增加Ra，Rd，HLGU和肌肉P-Akt / Akt，而不会影响血糖，FBF，MXD肝脏或主动脉P-Akt / Akt。渥曼青霉素可阻止FBF，MXD和肝脏P-Akt / Akt从10 mU.min-1.kg-1胰岛素增加。单独比较渥曼青霉素+10 mU.min-1.kg-1胰岛素和20 mU.min-1.kg-1胰岛素（两者均约为5,000 pM PI）显示，渥曼青霉素完全阻断了FBF和Ra的变化，部分阻断了GIR，Ra，Rd，HLGU和肌肉P-AKT / Akt。总之，渥曼青霉素在体内可增加血浆胰岛素，并完全抑制肝脏和主动脉以及部分肌肉中胰岛素介导的作用，后者可能是由于抑制胰岛素介导的血流量增加和毛细血管募集而引起的。

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