Reimann M, Qin N, Gruber M, Bornstein S R, Kirschbaum C, Ziemssen T, Eisenhofer G
Autonomic and Neuroendocrinological Laboratory Dresden, Center of Clinical Neuroscience, Department of Neurology, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden Germany.
Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Int J Obes (Lond). 2017 May;41(5):714-721. doi: 10.1038/ijo.2017.36. Epub 2017 Feb 6.
Although there is strong evidence linking obesity with increased sympathoneural activity, involvement of the adrenal medulla is less clear. We therefore investigated adrenal medullary function under fasting and feeding conditions in normal weight (NW, n=33), overweight (OW, n=28) and obese (OB, n=36) adults (59% women).
Ninety-seven healthy adults participated in a cross-sectional study with recruitment stratified according to BMI. Plasma for catecholamines and metanephrines was sampled in the fasting state, at 30-min intervals during a 120-min glucose tolerance test and during an euglycaemic-hyperinsulinaemic clamp (40 mU m min insulin dose). Body composition was determined by leg-to-leg bioelectrical impedance analysis.
Obese subjects had the lowest fasting plasma concentrations of epinephrine (NW: 0.17, 95% confidence interval (CI): 0.14-0.20 nmol l; OW: 0.16, 95% CI: 0.12-0.19 nmol l; OB: 0.11, 95% CI: 0.08-0.13 nmol l; P=0.018) and metanephrine (NW: 0.17, 95% CI: 0.15-0.19 nmol l; OW: 0.15, 95% CI: 0.13-0.16 nmol l; OB: 0.13, 95% CI: 0.12-0.15 nmol l; P=0.022), the latter reflecting adrenal medullary store size. Fasting plasma epinephrine (r=-0.437; P<0.001) and metanephrine (r=-0.477; P<0.001) concentrations were additionally inversely correlated with whole-body fat percentage. Suppression of epinephrine secretion in response to carbohydrate ingestion was significantly blunted in overweight and obese subjects compared with the normal weight subjects (P=0.045). Most of the variance in basal epinephrine was related to whole-body fat percentage (β=-0.389, 95% CI: -0.09 to -0.69; P=0.012) that explained the lower concentrations of epinephrine and metanephrine in women than men.
We provide evidence that adrenomedullary dysfunction is a characteristic feature of obesity that involves both reduced adrenal secretion of epinephrine and size of adrenal medullary epinephrine stores.
尽管有充分证据表明肥胖与交感神经活动增强有关,但肾上腺髓质在其中的作用尚不清楚。因此,我们研究了正常体重(NW,n = 33)、超重(OW,n = 28)和肥胖(OB,n = 36)成年人(59%为女性)在禁食和进食条件下的肾上腺髓质功能。
97名健康成年人参与了一项横断面研究,根据BMI进行分层招募。在禁食状态下、120分钟葡萄糖耐量试验期间每隔30分钟以及在正常血糖-高胰岛素钳夹试验(胰岛素剂量为40 mU m min)期间采集儿茶酚胺和甲氧基肾上腺素的血浆样本。通过双腿生物电阻抗分析测定身体成分。
肥胖受试者的空腹血浆肾上腺素浓度最低(NW:0.17,95%置信区间(CI):0.14 - 0.20 nmol/l;OW:0.16,95% CI:0.12 - 0.19 nmol/l;OB:0.11,95% CI:0.08 - 0.13 nmol/l;P = 0.018)和甲氧基肾上腺素浓度最低(NW:0.17,95% CI:0.15 - 0.19 nmol/l;OW:0.15,95% CI:0.13 - 0.16 nmol/l;OB:0.13,95% CI:0.12 - 0.15 nmol/l;P = 0.022),后者反映肾上腺髓质储存量大小。空腹血浆肾上腺素(r = -0.437;P < 0.001)和甲氧基肾上腺素(r = -0.477;P < 0.001)浓度还与全身脂肪百分比呈负相关。与正常体重受试者相比,超重和肥胖受试者对碳水化合物摄入的肾上腺素分泌抑制明显减弱(P = 0.045)。基础肾上腺素的大部分变异与全身脂肪百分比有关(β = -0.389,95% CI:-0.09至-0.69;P = 0.012),这解释了女性肾上腺素和甲氧基肾上腺素浓度低于男性的原因。
我们提供的证据表明,肾上腺髓质功能障碍是肥胖的一个特征,涉及肾上腺素的肾上腺分泌减少以及肾上腺髓质肾上腺素储存量减小。