Division of Cardiovascular Sciences, School of Medical Sciences, Core Technology Facility, University of Manchester, Manchester, UK.
Manchester Diabetes Centre, Manchester University Foundation Trust, Manchester, UK.
Int J Obes (Lond). 2021 Mar;45(3):631-638. doi: 10.1038/s41366-020-00727-9. Epub 2021 Jan 27.
Subjects with obesity have metabolic risk factors for nerve fibre damage. Because bariatric surgery improves these risk factors we have assessed whether this can ameliorate nerve fibre damage.
Twenty-six obese subjects without diabetes (age: 46.23 ± 8.6, BMI: 48.7 ± 1.5, HbA1c: 38.0 ± 4.5) and 20 controls (age: 48.3 ± 6.2, BMI: 26.8 ± 4.2, HbA1c: 39.1 ± 2.6) underwent detailed assessment of neuropathy at baseline and 12 months after bariatric surgery.
Obese subjects had normal peroneal (45.9 ± 5.5 vs. 48.1 ± 4.5, P = 0.1) and sural (46.9 ± 7.6 vs. 47.9 ± 10.6, P = 0.1) nerve conduction velocity, but a significantly higher neuropathy symptom profile (NSP) (4.3 ± 5.7 vs. 0.3 ± 0.6, P = 0.001), vibration perception threshold (VPT) (V) (10.2 ± 6.8 vs. 4.8 ± 2.7, P < 0.0001), warm threshold (C°) (40.4 ± 3.5 vs. 37.2 ± 1.8, P = 0.003) and lower peroneal (3.8 ± 2.2 vs. 4.9 ± 2.2, P = 0.02) and sural (8.9 ± 5.8 vs. 15.2 ± 8.5, P < 0.0001) nerve amplitude, deep breathing-heart rate variability (DB-HRV) (beats/min) (21.7 ± 4.1 vs. 30.1 ± 14, P = 0.001), corneal nerve fibre density (CNFD) (n/mm) (25.6 ± 5.3 vs. 32.0 ± 3.1, P < 0.0001), corneal nerve branch density (CNBD) (n/mm) (56.9 ± 27.5 vs. 111.4 ± 30.7, P < 0.0001) and corneal nerve fibre length (CNFL) (mm/mm) (17.9 ± 4.1 vs. 29.8 ± 4.9, P < 0.0001) compared to controls at baseline. In control subjects there was no change in neuropathy measures over 12 months. However, 12 months after bariatric surgery there was a significant reduction in BMI (33.7 ± 1.7 vs. 48.7 ± 1.5, P = 0.001), HbA1c (34.3 ± 0.6 vs. 38.0 ± 4.5, P = 0.0002), triglycerides (mmol/l) (1.3 ± 0.6 vs. 1.6 ± 0.8, P = 0.005) and low-density lipoprotein cholesterol (mmol/l) (2.7 ± 0.7 vs. 3.1 ± 0.9, P = 0.02) and an increase in high-density lipoprotein cholesterol (mmol/l) (1.2 ± 0.3 vs. 1.04 ± 0.2, P = 0.002). There was a significant improvement in NSP (1.6 ± 2.7 vs. 4.3 ± 5.7, P = 0.004), neuropathy disability score (0.3 ± 0.9 vs. 1.3 ± 2.0, P = 0.03), CNFD (28.2 ± 4.4 vs. 25.6 ± 5.3, P = 0.03), CNBD (64.7 ± 26.1 vs. 56.9 ± 27.5, P = 0.04) and CNFL (20.4 ± 1.2 vs. 17.9 ± 4.1, P = 0.02), but no change in cold and warm threshold, VPT, DB-HRV or nerve conduction velocity and amplitude. Increase in CNFD correlated with a decrease in triglycerides (r = -0.45, P = 0.04).
Obese subjects have evidence of neuropathy, and bariatric surgery leads to an improvement in weight, HbA1c, lipids, neuropathic symptoms and deficits and small nerve fibre regeneration without a change in quantitative sensory testing, autonomic function or neurophysiology.
肥胖者存在神经纤维损伤的代谢风险因素。由于减重手术改善了这些风险因素,我们评估了这是否可以改善神经纤维损伤。
26 名无糖尿病的肥胖受试者(年龄:46.23±8.6,BMI:48.7±1.5,HbA1c:38.0±4.5)和 20 名对照者(年龄:48.3±6.2,BMI:26.8±4.2,HbA1c:39.1±2.6)在减重手术后 12 个月进行了详细的神经病变评估。
肥胖受试者的腓总神经(45.9±5.5 与 48.1±4.5,P=0.1)和腓肠神经(46.9±7.6 与 47.9±10.6,P=0.1)的神经传导速度正常,但神经病变症状评分(NSP)(4.3±5.7 与 0.3±0.6,P=0.001)、振动感觉阈值(VPT)(V)(10.2±6.8 与 4.8±2.7,P<0.0001)、温暖阈值(C°)(40.4±3.5 与 37.2±1.8,P=0.003)和腓肠神经(3.8±2.2 与 4.9±2.2,P=0.02)和腓肠神经(8.9±5.8 与 15.2±8.5,P<0.0001)的振幅较低,深呼吸心率变异性(DB-HRV)(次/分钟)(21.7±4.1 与 30.1±14,P=0.001)、角膜神经纤维密度(CNFD)(个/mm)(25.6±5.3 与 32.0±3.1,P<0.0001)、角膜神经分支密度(CNBD)(个/mm)(56.9±27.5 与 111.4±30.7,P<0.0001)和角膜神经纤维长度(CNFL)(mm/mm)(17.9±4.1 与 29.8±4.9,P<0.0001)与对照组相比均较低。在对照组中,12 个月内神经病变测量值没有变化。然而,减重手术后 12 个月,BMI(33.7±1.7 与 48.7±1.5,P=0.001)、HbA1c(34.3±0.6 与 38.0±4.5,P=0.0002)、甘油三酯(mmol/l)(1.3±0.6 与 1.6±0.8,P=0.005)和低密度脂蛋白胆固醇(mmol/l)(2.7±0.7 与 3.1±0.9,P=0.02)降低,高密度脂蛋白胆固醇(mmol/l)(1.2±0.3 与 1.04±0.2,P=0.002)升高。NSP(1.6±2.7 与 4.3±5.7,P=0.004)、神经病变残疾评分(0.3±0.9 与 1.3±2.0,P=0.03)、CNFD(28.2±4.4 与 25.6±5.3,P=0.03)、CNBD(64.7±26.1 与 56.9±27.5,P=0.04)和 CNFL(20.4±1.2 与 17.9±4.1,P=0.02)显著改善,但冷、温暖阈值、VPT、DB-HRV 或神经传导速度和幅度无变化。CNFD 的增加与甘油三酯的减少相关(r=-0.45,P=0.04)。
肥胖者存在神经病变,减重手术可改善体重、HbA1c、血脂、神经病变症状和缺陷,并促进小纤维神经再生,而定量感觉测试、自主功能或神经生理学无变化。