Oral glucose tolerance test-induced increases in femoral blood flow are absent in nonobese females with polycystic ovary syndrome.

IF 3.1 2区 医学 Q1 ENDOCRINOLOGY & METABOLISM
Danielle E Berbrier, Will Huckins, Emily K Van Berkel, Shannon I Delage, Sarkis J Hannaian, Raychel Myara, Oluwakanyisola N Okafor, Ta Heh Chung, Togas Tulandi, Shauna L Reinblatt, Rachel N Lord, Tyler A Churchward-Venne, Charlotte W Usselman
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Abstract

The oral glucose tolerance test (OGTT) promotes transient increases in peripheral blood flow via humoral mechanisms, including insulin. Polycystic ovary syndrome (PCOS) is associated with insulin resistance and vascular dysfunction, even in nonobese females. We therefore tested the hypothesis that OGTT-stimulated increases in femoral blood flow (FBF) would be impaired in females with PCOS. In the overnight postabsorptive state, plasma glucose, insulin, and FBF (duplex ultrasound and superficial femoral artery) were measured pre-OGTT and at 0, 15, 30, 60, 90, and 120 min following a 75-g glucose bolus. We recruited females with PCOS [n = 10, age: 27 ± 5 yr, body mass index (BMI): 23.8 ± 3.1 kg/m2] and age- and BMI-matched females without PCOS (CTRL; n = 10, age: 27 ± 4 yr, BMI: 23.7 ± 2.0 kg/m2). Pre-OGTT glucose concentrations were not different between PCOS and CTRL (4.7 ± 0.4 vs. 4.7 ± 0.4 mmol/L, P = 0.74), nor were insulin concentrations (41.7 ± 12.0 vs. 32.4 ± 11.2 pmol/L, P = 0.11). However, OGTT glucose area under the curve (AUC; 938 ± 124 vs. 762 ± 113 mmol/L × 120 min, P = 0.01) and insulin AUC (45,121 ± 16,204 vs. 27,079 ± 11,527 pmol/L × 120 min, P = 0.01) were higher in PCOS than CTRL. Pre-OGTT, FBF was not different between PCOS and CTRL (211 ± 50 vs. 210 ± 44 mL/min, P = 0.95). FBF increased across all time points postbolus in CTRL but remained unchanged in PCOS (OGTT × group, P < 0.01). Indeed, FBF was lower in PCOS than CTRL at 30 (224 ± 33 vs. 277 ± 48 mL/min, P = 0.01), 60 (227 ± 37 vs. 305 ± 48 mL/min, P < 0.01), 90 (217 ± 45 vs. 308 ± 64 mL/min, P < 0.01), and 120 min (205 ± 47 vs. 258 ± 55 mL/min, P = 0.04) postbolus. In sum, nonobese females with PCOS demonstrated a complete absence of OGTT-stimulated increases in peripheral artery blood flow, suggesting that PCOS is associated with profound vascular dysfunction following acute hyperglycemia.NEW & NOTEWORTHY To the best of our knowledge, this is the first study to demonstrate that nonobese females with polycystic ovary syndrome (PCOS) do not exhibit oral glucose tolerance test-induced increases in peripheral blood flow, unlike healthy controls. These findings highlight the peripheral vasculature as a critical and overlooked component of cardiometabolic dysfunction in PCOS, even in the absence of obesity and other cardiometabolic risk factors (e.g., hypertension and diabetes).

口服糖耐量试验诱导的股骨血流增加在患有多囊卵巢综合征的非肥胖女性中不存在。
口服葡萄糖耐量试验(OGTT)通过包括胰岛素在内的体液机制促进外周血流量的短暂增加。多囊卵巢综合征(PCOS)与胰岛素抵抗和血管功能障碍有关,即使在非肥胖女性中也是如此。因此,我们验证了ogtt刺激的股骨血流量(FBF)增加会损害PCOS女性患者的假设。在一夜吸收后状态下,在ogtt前和75 g葡萄糖后0、15、30、60、90、120分钟测量血浆葡萄糖、胰岛素和FBF(双相超声,股浅动脉)。我们招募了患有PCOS的女性(n=10,年龄:27±5岁,体重指数(BMI): 23.8±3.1kg/m2)和年龄与BMI匹配的非PCOS女性(n=10,年龄:27±4岁,BMI: 23.7±2.0kg/m2)。ogtt前葡萄糖浓度在PCOS和CTRL组之间无差异(4.7±0.4 vs 4.7±0.4mmol/L, P=0.74),胰岛素浓度也无差异(41.7±12.0 vs 32.4±11.2pmol/L, P=0.11)。PCOS组OGTT葡萄糖曲线下面积(AUC; 938±124 vs 762±113mmol/Lx120min, P=0.01)和胰岛素AUC(45121±16204 vs 27079±11527pmol/Lx120min, P=0.01)高于对照组。ogtt前,PCOS组与对照组FBF差异无统计学意义(211±50 vs 210±44mL/min, P=0.95)。FBF在CTRL组注射后的所有时间点均有所增加,但在PCOS组保持不变(OGTT x组,P)。事实上,PCOS患者FBF在服药后30分钟(224±33 vs 277±48mL/min, P=0.01)、60分钟(227±37 vs 305±48mL/min, P)、90分钟(217±45 vs 308±64mL/min, P)和120分钟(205±47 vs 258±55mL/min, P=0.04)时均低于对照组。总之,患有多囊卵巢综合征的非肥胖女性完全没有ogtt刺激的外周动脉血流增加,这表明多囊卵巢综合征与急性高血糖后的严重血管功能障碍有关。
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来源期刊
CiteScore
9.80
自引率
0.00%
发文量
98
审稿时长
1 months
期刊介绍: The American Journal of Physiology-Endocrinology and Metabolism publishes original, mechanistic studies on the physiology of endocrine and metabolic systems. Physiological, cellular, and molecular studies in whole animals or humans will be considered. Specific themes include, but are not limited to, mechanisms of hormone and growth factor action; hormonal and nutritional regulation of metabolism, inflammation, microbiome and energy balance; integrative organ cross talk; paracrine and autocrine control of endocrine cells; function and activation of hormone receptors; endocrine or metabolic control of channels, transporters, and membrane function; temporal analysis of hormone secretion and metabolism; and mathematical/kinetic modeling of metabolism. Novel molecular, immunological, or biophysical studies of hormone action are also welcome.
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