Multiple additive moderation effects of insulin resistance and dietary inflammatory index on the relationship between body mass index and postprandial glucose levels in Korea: a retrospective analysis
- Author:
Jiwon PARK
1
;
Myoung Soo KIM
Author Information
- Publication Type:Original Article
- From:Journal of Korean Biological Nursing Science 2025;27(2):284-294
- CountryRepublic of Korea
- Language:English
- Abstract: This study examined the potential moderating effects of insulin resistance and dietary inflammatory index (DII) on the relationship between body mass index (BMI) and peak postprandial glucose levels in patients with prediabetes and type 2 diabetes. Methods: A retrospective analysis was conducted, using integrated nutritional data from a diabetes management program for patients with prediabetes and type 2 diabetes who used continuous glucose monitoring (CGM). Data from 17 patients, including 408 meal records, were analyzed. The energy-adjusted DII (E-DII) was calculated, and peak postprandial glucose was matched for each meal. Statistical tests analyzed differences and relationships between variables. Hayes' SPSS PROCESS macro version 4.0 was used to identify the moderating effects. Results: Peak postprandial glucose levels varied significantly among E-DII subgroups (p < .026) and were positively correlated with insulin resistance (rho = .30, p = < .001) and E-DII (rho = .14, p = .004). Insulin resistance and E-DII had a multiple additive moderating effect on the relationship between BMI and peak postprandial glucose levels in glucose-controlled patients (F = 12.22, p < .001), explaining 21.6% of the variance. Conclusion: Higher E-DII scores, which indicated a more pro-inflammatory diet, were associated with increased glucose levels, especially for patients who were overweight and mildly obese. Patients with obesity who received insulin therapy had varied postprandial glucose levels depending on their insulin resistance status. These findings highlight the importance of tailored dietary interventions, inflammation management, and CGM to improve obesity-related glucose regulation.
