2239-P: Association of the Metabolic Score for Visceral Fat and Prediabetes Development in China: Evidence from a Nationwide Chinese Cohort Study

Introduction and Objective: The Metabolic Score for Visceral Fat (METS-VF) is an effective indicator of visceral adipose tissue (VAT). This study aimed to explore the association between METS-VF and prediabetes development in middle-aged and elderly adults in China. Methods: This study used data from the China Health and Retirement Longitudinal Study (CHARLS) 2011 (baseline) and 2015 (endpoint) waves. The associations between baseline METS-VF, cumulative METS-VF (cumMETS-VF), METS-VF changes and prediabetes development (progression to diabetes or regression to normoglycemia) were explored using Cox regression and restricted cubic spline (RCS) models. Subgroup analyses and interaction tests were also conducted. Results: A total of 2,143 participants with prediabetes at baseline were enrolled. Over 3 years follow-up, 12.93% progressed to diabetes, while 23.28% regressed to normoglycemia. Baseline METS-VF and cumMETS-VF were positively associated with prediabetes progression [HRs (95% CIs) 2.126 (1.576-2.868), 1.351 (1.215-1.503)], and negatively associated with regression to normoglycemia [HRs (95% CIs) 0.757 (0.637-0.899), 0.902 (0.849-0.959)]. Additionally, compared to individuals with consistently-low METS-VF, those with low-to-high and consistently-high METS-VF had a 63.4% and 141.2% higher risk of prediabetes progression. In contrast, the probability of regression to normoglycemia decreased by 23.4% in the consistently-high group. Moreover, RCS analysis demonstrated a nonlinear relationship between cumMETS-VF and prediabetes progression. Among individuals with BMI>24kg/m², higher baseline METS-VF was significantly associated with a reduced likelihood of prediabetes regression (P interaction<0.05). Conclusion: METS-VF is correlated with the prediabetes development among middle-aged and elderly adults in China. High METS-VF significantly increased the risk of progression to diabetes and hindered the regression to normolycemia.