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升压剂量的血管紧张素II可增加血压正常男性中胰岛素介导的葡萄糖摄取。

Pressor doses of angiotensin II increase insulin-mediated glucose uptake in normotensive men.

作者信息

Townsend R R, DiPette D J

机构信息

Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555-0566.

出版信息

Am J Physiol. 1993 Sep;265(3 Pt 1):E362-6. doi: 10.1152/ajpendo.1993.265.3.E362.

Abstract

The effect of pressor doses of angiotensin II infused intravenously on insulin-mediated glucose uptake was determined in normotensive men. A 3-h hyperinsulinemic euglycemic clamp was employed in 14 normotensive subjects to determine insulin-mediated glucose uptake with or without an infusion of angiotensin II (approximately 15 ng.kg-1.min-1), which increased blood pressure by 20/15 mmHg (systolic/diastolic). Addition of angiotensin II increased whole body glucose uptake by 15% (9.2 +/- 0.5 vs. 10.8 +/- 0.8 mg.kg-1 x min-1; P = 0.011), and glucose oxidation (determined by indirect calorimetry) by 25% (4.0 +/- 0.3 vs. 4.9 +/- 0.4 mg.kg-1 x min-1; P < 0.05) over insulin alone. There was no significant increase in hepatic glucose output during angiotensin II infusion (2.2 +/- 0.1 vs. 2.4 +/- 0.1 mg.kg-1 x min-1; P = NS). We conclude that angiotensin II in pressor doses increases insulin-mediated glucose disposal and oxidation. The mechanism for this may involve a redirection of blood flow into skeletal muscle during angiotensin II infusion or a direct biochemical action of angiotensin II. Although performed in lean normotensive subjects, these results cast doubt on a significant role for angiotensin II in the insulin resistance associated with essential hypertension.

摘要

在血压正常的男性中,测定了静脉注射升压剂量的血管紧张素II对胰岛素介导的葡萄糖摄取的影响。对14名血压正常的受试者采用3小时高胰岛素正常血糖钳夹技术,以测定在输注或不输注血管紧张素II(约15 ng·kg-1·min-1)情况下胰岛素介导的葡萄糖摄取,输注血管紧张素II使血压升高20/15 mmHg(收缩压/舒张压)。添加血管紧张素II后,全身葡萄糖摄取增加了15%(9.2±0.5对10.8±0.8 mg·kg-1·min-1;P = 0.011),葡萄糖氧化(通过间接测热法测定)比单独使用胰岛素时增加了25%(4.0±0.3对4.9±0.4 mg·kg-1·min-1;P < 0.05)。在输注血管紧张素II期间,肝脏葡萄糖输出没有显著增加(2.2±0.1对2.4±0.1 mg·kg-1·min-1;P = 无显著性差异)。我们得出结论,升压剂量的血管紧张素II可增加胰岛素介导的葡萄糖处置和氧化。其机制可能涉及在输注血管紧张素II期间血流重新导向骨骼肌,或血管紧张素II的直接生化作用。尽管这些研究是在体型偏瘦、血压正常的受试者中进行的,但这些结果对血管紧张素II在原发性高血压相关胰岛素抵抗中的重要作用提出了质疑。

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