188-OR: Inflammatory and Insulinemic Dietary Patterns Associate with Nephropathy in Type 1 Diabetes (T1D)

Abstract

Diabetic nephropathy (DN) causes much morbidity and mortality in T1D, necessitating better mechanistic insights for improved prevention and therapy. In addition to hyperglycemia, DN pathogenesis may involve inflammation or insulin resistance, and diets modulating these pathways may impact DN risk. In this cross-sectional study, we examined associations of inflammatory and insulinemic potentials of whole diets with DN in a subset of the Joslin 50-year Medalist Study, comprising 570 individuals with T1D >50 years and food frequency questionnaire data. Empirical dietary inflammatory pattern (EDIP) and empirical index for hyperinsulinemia (EDIH) scores were separately derived as weighted sums of foods and beverages previously shown to be predictive of circulating inflammatory biomarkers or C-peptide levels, respectively. In multivariable-adjusted logistic regression models, including age, sex, BMI, exercise, lipids, HbA1c, and hypertension as covariates, 1 S.D. increments in EDIP and EDIH associated with 0.46 (95% CI 0.26-0.84, p=0.01) and 0.31 (95% CI 0.15-0.68, p=0.003) reduced odds of being protected against DN (167 events, CKD-EPI eGFR < 60 ml/min/1.73 m2), respectively. Both scores inversely correlated with continuous eGFR (p=0.03 and 0.0003, respectively). Neither index associated with HbA1c, retinopathy severity, neuropathy or cardiovascular diseases. Both scores positively correlated (p<0.05) with C-reactive protein, which correlated to HbA1c but did not offset the effects of EDIP or EDIH on DN. These findings show that dietary patterns with higher inflammatory and insulinemic potentials are associated with DN in T1D, independent of glycemic control, inflammation or hypertension, suggesting the involvement of a metabolic and renal-selective pathway underlying DN pathogenesis. Future studies will focus on whether consumption of diets with low EDIP and EDIH can protect against DN onset and progression, and the potential pathways through which they do this. Disclosure H. Shah: None. A. Adam: None. T. Boumenna: None. M. Yu: None. J. Li: None. F. Hu: None. F. K. Tabung: None. G. L. King: Consultant; Self; Agios, Inc., Medtronic, Other Relationship; Self; Janssen Pharmaceuticals, Inc.