Bariatric surgery leads to an improvement in small nerve fibre damage in subjects with obesity

• Published in: International Journal of Obesity Vol. 45; no. 3; pp. 631 - 638
• Main Authors: Azmi, Shazli, Ferdousi, Maryam, Liu, Yifen, Adam, Safwaan, Iqbal, Zohaib, Dhage, Shaishav, Ponirakis, Georgios, Siahmansur, Tarza, Marshall, Andrew, Petropoulos, Ioannis, Kalteniece, Alise, Ho, Jan Hoong, Syed, Akheel, Gibson, John M., Ammori, Basil J., Durrington, Paul N., Malik, Rayaz A., Soran, Handrean
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.03.2021; Nature Publishing Group
• Subjects: 42/56; 692/308/2779/109/2154; 692/699/2743/393; Adult; Amplitudes; Autonomic nervous system; Bariatric Surgery - statistics & numerical data; Care and treatment; Cholesterol; Cohort Studies; Complications and side effects; Cornea; Cornea - innervation; Cornea - physiology; Damage; Density; Diabetes mellitus; Diabetic neuropathy; Epidemiology; Erythromelalgia; Female; Gastrointestinal surgery; Health Promotion and Disease Prevention; Heart rate; Humans; Internal Medicine; Lipids; Male; Medicine; Medicine & Public Health; Metabolic Diseases; Middle Aged; Nerve conduction; Nerve Fibers - physiology; Neurophysiology; Obesity; Obesity - physiopathology; Obesity - surgery; Patient outcomes; Public Health; Regeneration; Risk analysis; Risk factors; Sensory evaluation; Sensory testing; Surgery; Triglycerides; Velocity; Vibration perception; United Kingdom
• ISSN: 0307-0565; 1476-5497; 1476-5497
• DOI: 10.1038/s41366-020-00727-9

Introduction 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. Methods 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. Results 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 2 ) (25.6 ± 5.3 vs. 32.0 ± 3.1, P  < 0.0001), corneal nerve branch density (CNBD) (n/mm 2 ) (56.9 ± 27.5 vs. 111.4 ± 30.7, P  < 0.0001) and corneal nerve fibre length (CNFL) (mm/mm 2 ) (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). Conclusion 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.