208-OR: Fat Mass and Insulin Resistance Are Independent Risk Factors for Polyneuropathy in Non-DM Subjects Who Underwent Bariatric/Metabolic Surgery

• Published in: Diabetes (New York, N.Y.) Vol. 70; no. Supplement_1
• Main Authors: KIM, KYUHO, OH, TAE JUNG, CHOI, SUNGHEE, JANG, HAK CHUL
• Format: Journal Article
• Language: English
• Published: New York American Diabetes Association 01.06.2021
• Subjects: Body fat; Body weight; Body weight loss; Computed tomography; Diabetes; Gastrointestinal surgery; Insulin; Insulin resistance; Metabolic syndrome; Metabolism; Neuropathy; Obesity; Polyneuropathy; Regression analysis; Risk factors; Surgery; Weight control
• ISSN: 0012-1797; 1939-327X
• DOI: 10.2337/db21-208-OR

Background: Obesity is an important risk factor for polyneuropathy (PN) in subjects with DM. However, PN can be detected in subjects without overt DM but with risk factors for DM such as metabolic syndrome. Therefore, it is worthy to investigate the prevalence of PN in obese subjects and to discover the underlying mechanisms of the association between obesity and PN. Methods: We analyzed the data of 184 subjects who underwent bariatric/metabolic surgery. PN was diagnosed when a Michigan Neuropathy Screening Instrument score was ≥ 2.5. Total body fat mass and percentage were measured by bioimpedance analysis, and visceral fat area (VFA) was quantified by computed tomography. According to DM status, obesity-related parameters were compared between subjects with PN and those without PN. The association between obesity-related parameters and PN was analyzed using logistic regression models. Results: Of 184 subjects (mean age, 39.1 years; mean BMI, 38.6 kg/m2), 39.7% were diagnosed with DM. The prevalence of PN was 9.0% in non-DM group and 21.9% in DM group. In non-DM group, subjects with PN showed higher HOMA-IR, fat mass, and VFA compared with those without PN. HOMA-IR (OR, 1.492; 95% CI, 1.110-2.005), fat mass (OR, 1.087; 95% CI, 1.008-1.171), and VFA (OR 1.013; 95% 1.001-1.024) were significantly associated with PN even after adjustment of known risk factors of PN. In DM group, subjects with PN showed higher body weight, BMI, waist circumference, and VFA compared with those without PN. However, after adjustment of known risk factors of PN, these obesity related parameters were not significantly associated with PN. Conclusion: Fat mass and insulin resistance might be independent risk factors in development of PN for obese subjects without DM. PN evaluation might be necessary in subjects with morbid obesity even before development of overt DM, and we need to investigate whether weight loss intervention can prevent or delay PN in obese subjects.