Abstract 075: Diurnal postprandial glucose responses to meals with different carbohydrate content and glycemic index and their effects on lipid metabolomics: The OmniCarb trial

Abstract

Background and aims: Meal timing has been suggested as a circadian disruptor that may be linked cardiovascular disease by influencing fatty acid metabolism and specific metabolomic pathways. We aimed to test associations of diurnal postprandial glucose responses (PPGRs) after consuming diets varying in carbohydrate amount (Carb) and glycemic index (GI) with comprehensive lipid subtypes and lipidomic signatures. Materials and methods: This ancillary analysis included 61 adults from the OmniCarb trial, a randomized crossover, controlled feeding trial of 4 diets that differed in Carb and GI levels. Each diet was based on a healthful DASH-type diet and was provided for 5 weeks, with a 2-week washout. Twelve-hour meal tests were conducted at the end of each intervention. Participants were given the same diet type for that diet period for breakfast, lunch, and dinner, which had a mean 486, 610, 618 kcal, respectively, for a typical 2000-kcal diet. The area under the curve (AUC) of glucose after each meal was calculated and analyses were performed per 1 SD higher of AUC-glucose. Lipid subtypes considering the presence of apolipoprotein C-III (apoC-III) were measured in fasting samples collected at the end of the intervention. Serum lipid metabolites were analyzed using Metabolon's complex lipids targeted panel. Results: At the end of high-carb and high-GI diet interventions, PPGRs after dinner, but not after lunch, were associated with higher levels of atherogenic apoC-III (β [SE]: 0.3 [0.1]; p=0.035), apoB (β 0.2 [0.1]; p=0.04), and cholesterol (β 1.2 [0.5]; p=0.018) in LDL with apoC-III. PPGRs after breakfast were not significantly related to cholesterol in LDL with apoC-III. When analyzing effects on lipid class concentrations, a low-carb and low-GI diet compared to high-carb and high-GI diet lowered triacylglycerol (TAG) and phosphatidylcholines but slightly increased phosphatidylethanolamines (PE) and lactosylceramides ( p <0.05 for all). At the end of low-carb and low-GI diet interventions, greater AUC-glucose after dinner and AUC-glucose differences between lunch and dinner showed significant associations with higher levels of cholesteryl esters, dihydroceramides, TAG, and PE. Conclusion: Greater PPGRs were associated with atherogenic lipid subtypes and lipidomic pathways after evening meals but not after daytime meals. The atherogenic lipid pathways associated with PPGRs in the evening may vary depending on Carb content and dietary GI of the meals.