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肥胖会削弱胰岛素介导的人体前臂肌肉微血管募集。

Obesity blunts insulin-mediated microvascular recruitment in human forearm muscle.

作者信息

Clerk Lucy H, Vincent Michelle A, Jahn Linda A, Liu Zhenqi, Lindner Jonathan R, Barrett Eugene J

机构信息

Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Virginia Health System, P.O. Box 801410, 450 Ray C. Hunt Drive, Charlottesville, VA 22908, USA.

出版信息

Diabetes. 2006 May;55(5):1436-42. doi: 10.2337/db05-1373.

Abstract

We have previously shown that skeletal muscle capillaries are rapidly recruited by physiological doses of insulin in both humans and animals. This facilitates glucose and insulin delivery to muscle, thus augmenting glucose uptake. In obese rats, both insulin-mediated microvascular recruitment and glucose uptake are diminished; however, this action of insulin has not been studied in obese humans. Here we used contrast ultrasound to measure microvascular blood volume (MBV) (an index of microvascular recruitment) in the forearm flexor muscles of lean and obese adults before and after a 120-min euglycemic-hyperinsulinemic (1 mU . min(-1) . kg(-1)) clamp. We also measured brachial artery flow, fasting lipid profile, and anthropomorphic variables. Fasting plasma glucose (5.4 +/- 0.1 vs. 5.1 +/- 0.1 mmol/l, P = 0.05), insulin (79 +/- 11 vs. 38 +/- 6 pmol/l, P = 0.003), and percent body fat (44 +/- 2 vs. 25 +/- 2%, P = 0.001) were higher in the obese than the lean adults. After 2 h of insulin infusion, whole-body glucose infusion rate was significantly lower in the obese versus lean group (19.3 +/- 3.2 and 37.4 +/- 2.6 mumol . min(-1) . kg(-1) respectively, P < 0.001). Compared with baseline, insulin increased MBV in the lean (18.7 +/- 3.3 to 25.0 +/- 4.1, P = 0.019) but not in the obese group (20.4 +/- 3.6 to 18.8 +/- 3.8, NS). Insulin increased brachial artery diameter and flow in the lean but not in the obese group. We observed a significant, negative correlation between DeltaMBV and BMI (R = -0.482, P = 0.027) in response to insulin. In conclusion, obesity eliminated the insulin-stimulated muscle microvascular recruitment and increased brachial artery blood flow seen in lean individuals.

摘要

我们之前已经表明,在人类和动物中,生理剂量的胰岛素可迅速促使骨骼肌毛细血管开放。这有助于葡萄糖和胰岛素输送至肌肉,从而增加葡萄糖摄取。在肥胖大鼠中,胰岛素介导的微血管开放和葡萄糖摄取均减少;然而,胰岛素的这一作用尚未在肥胖人类中得到研究。在此,我们使用对比超声测量了体重正常和肥胖成年人在120分钟正常血糖 - 高胰岛素血症(1 mU·min⁻¹·kg⁻¹)钳夹前后,前臂屈肌的微血管血容量(MBV,微血管开放的一个指标)。我们还测量了肱动脉血流、空腹血脂谱和人体测量学变量。肥胖成年人的空腹血糖(5.4±0.1 与 5.1±0.1 mmol/L,P = 0.05)、胰岛素(79±11 与 38±6 pmol/L,P = 0.003)和体脂百分比(44±2 与 25±2%,P = 0.001)均高于体重正常的成年人。胰岛素输注2小时后,肥胖组的全身葡萄糖输注率显著低于体重正常组(分别为19.3±3.2 和 37.4±2.6 μmol·min⁻¹·kg⁻¹,P < 0.001)。与基线相比,胰岛素使体重正常组的MBV增加(从18.7±3.3 增至 25.0±4.1,P = 0.019),但肥胖组未增加(从20.4±3.6 降至 18.8±3.8,无显著差异)。胰岛素使体重正常组的肱动脉直径和血流增加,但肥胖组未增加。我们观察到,胰岛素作用后,ΔMBV与BMI之间存在显著的负相关(R = -0.482,P = 0.027)。总之,肥胖消除了胰岛素刺激的肌肉微血管开放,并增加了体重正常个体中所见的肱动脉血流。

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