혈당조절 중재 중인 당뇨병 전단계 및 당뇨병 환자의 체질량지수와 식후최대혈당 간의 관계에서 인슐린 저항성, 식사염증지수의 다중가산조절효과

Abstract

Purpose Postprandial hyperglycemia is a risk factor for metabolic syndrome, diabetes, and cardiovascular disease. It is vital that the level of blood sugar is controlled and the morbidity and complications of other diseases are reduced long-term. Continuous glucose monitoring can easily detect postprandial hyperglycemia, so appropriate education and nutrient counseling can maximize this advantage. In particular, obese people are likely to have difficulties with glucose metabolism. Previous studies have found that body mass index, insulin resistance, and dietary inflammation index are factors that can increase postprandial glucose. Therefore, this study investigated whether insulin resistance and dietary inflammation index can modulate the relationship between body mass index and peak postprandial glucose.

Method This study used the integrated nutritional data of the project that evaluated the effectiveness of the diabetes management program for prediabetic and type 2 diabetic patients with continuous glucose monitoring. The study gathered 408 dietary data from seventeen patients (breakfast, lunch, or dinner). Each participant had twenty-four meal records; energy-adjusted dietary inflammatory index was calculated according to each meal, and peak postprandial glucose was matched. Insulin resistance was calculated by homeostasis model assessment of insulin resistance (HOMA-IR) and energy-adjusted dietary inflammatory index (E-DII) indicating the inflammatory potential of the overall diet was calculated based on thirty-one nutrition components' pro- and anti-inflammatory properties. Mann-Whitney U tests and Spearman's rank correlation coefficients were used to analyze differences and relationships among study variables. MACRO Process was used to identify multiple additive moderation effects of insulin resistance and dietary inflammatory index on the relationship between body mass index and postprandial glucose.

Result Peak postprandial glucose differed significantly among E-DII subgroups (p<.026). Positive correlations were observed between peak postprandial glucose and 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 prandial glucose among prediabetic and diabetic patients undergoing glucose control (F=12.22, p<.001); the explanatory power of the model was 21.6%. In the group with a body mass index of less than 30, peak postprandial blood glucose was found to increase as the E-DII and insulin resistance increased. In contrast, in the group with a body mass index of 30 or more, peak postprandial glucose lowered as E-DII increased in all groups with low insulin resistance, the middle and the high groups.

Conclusion Insulin resistance and dietary inflammatory index can modulate the relationship between body mass index and peak postprandial blood glucose. Mixed meals with a low dietary inflammatory index and insulin resistance can significantly reduce postprandial glucose in prediabetic and diabetic patients undergoing glucose control with BMI<30. The findings of this study shed light on the development of a lifestyle intervention program that educates obese people to reduce insulin resistance and dietary inflammatory index, leading to appropriate regulation of glucose levels.