Mechanism of Diabetes Remission or Improvement in Glucose Control Following Roux-en-Y Gastric Bypass Versus Sleeve Gastrectomy: A Systematic Review and Meta-Analysis

Abstract

Background: The mechanisms of diabetes remission following bariatric surgery independent of calorie restriction and weight loss remain unclear. Objectives: To undertake a systematic review and meta-analysis to investigate mechanisms underpinning diabetes remission. Methods: We included individuals with type 2 diabetes who have undergone RYGB, SG, and a very low-calorie diet (VLCD). In total, 234 studies were identified (N = 52 for qualitative; N = 40 for quantitative synthesis). Review Manager v5.4 and IBM SPSS for Windows (v28.0.1.1) were used for analysis. Results: Crude annualised diabetes relapse rates for RYGB and SG are as follows: −6.98 ± 16.19 (p = 0.046) and −2.75 ± 4.94 (p = 0.08); crude remission rates for RYGB and SG, respectively, are as follows: 39.59 ± 45.93 (p = 0.000) and 33.36 ± 33.87 SG (p = 0.006). Differences in other metabolic outcomes (standardised mean difference and 95% confidence intervals (CIs)) are BMI: ([RYGB: −2.73, 95%CI: −3.14 to −2.32, p < 0.000001) (SG: −2.82, 95%CI: −5.04 to −0.60, p = 0.01)]; HbA1c: [(RYGB: −1.58, 95%CI: −2.16 to −1.00, p < 0.00001) (SG: −1.42, 95%CI: −1.69 to −1.15, p < 0.00001)]; insulin: [(RYGB: 0.16, 95%CI: −0.19 to −0.50, p = 0.37) (SG: −3.00, 95%CI: −3.17 to −2.82, p = 0.75)]; and fat mass [(RYGB: −2.56, 95%CI: −4.49 to −0.64, p = 0.009) (SG: −1.69, 95%CI: −4.58 to 1.21, p = 0.25)]. RYGB and SG produced a significant improvement in HOMA-B measurements. Adiponectin and the Matsuda index were significantly increased with RYGB. No difference was observed for other metabolic markers (RYGB: GLP-1, GIP, leptin, ghrelin, PYY) (SG: GLP-1 and FGF19) (VLCD: leptin, GLP-1, GIP, and ghrelin). Conclusions: Diabetes remission following RYGB and SG was primarily driven by improvement in beta-cell function, with improvement in insulin resistance markers also observed for RYGB, driven by reductions in fat mass. No other metabolic mechanism explaining diabetes remission was observed based on clinical studies.