331-OR: Glycemic Index and Postprandial Blood Glucose Excursions, Insulin Requirements, and Hunger in T1D

Abstract

High compared to low glycemic index (GI) foods elicit larger glycemic and insulinemic excursions, and are associated with lower satiety. However, it is unclear whether the satiety effect is attributable to differences in glycemia or insulinemia, and whether insulin delivery in individuals with T1D could be optimized for satiety per se. Fifteen men with T1D, BMI 25 (SD 3) kg/m2, aged 23 (5) years, HbA1c 7.4 (0.7)% underwent three experimental conditions in a randomized cross-over design: High GI, high insulin (HGI/HI): meal GI of 84 with intravenous insulin (IVI) to maintain euglycemia; Low GI (LGI): meal GI of 37 with IVI to maintain euglycemia (comparison condition); High GI, low insulin (HGI/LI): high GI meal as above with IVI matched to LGI. Test meals provided 25% of daily calories (60% carbohydrate, 15% protein, 25% fat). IVI was adjusted using a PID algorithm with blood glucose measurements every 5 minutes for 4.5 hr. When using matched insulin doses, blood glucose area under the curve (AUC) was 789 (145) vs. 493 (48) mg/dl*h (p<0.001) for HGI/LI vs. LGI. To maintain euglycemia (HGI/HI vs. LGI), 25 (9) vs. 17 (5) units of insulin were needed (p=0.005). Late postprandial (3.5-4.5 hr) free fatty acid (FFA) concentrations were higher for HGI/HI (0.62 [0.31] mmol/L) vs. LGI (0.26 [0.09] mmol/L p=0.008). Hunger was lower at peak glycemia (1 hr) for HGI/HI vs. LGI (2.3 vs. 3.2 on a 0-10 scale, p=0.01), but was greater in the late postprandial phase after either HGI/HI or HGI/LI vs. LGI (6.3 [p=0.05] or 6.3 [p=0.03] vs. 5.3, respectively). In a controlled feeding study, a high GI meal was associated with a 1.5-fold higher insulin requirement to obtain similar glycemia, or a 1.6-fold higher glucose AUC when using the same insulin dose. The high GI meal also increased late postprandial hunger regardless of insulin dose, and resulted in a greater rise in FFA (high insulin condition). These meal effects, with or without aggressive insulin management, may predispose to cardiovascular risk, metabolic dysfunction or weight gain. Disclosure B.S. Lennerz: None. D.C. Simonson: Stock/Shareholder; Self; GI Windows, Inc. Stock/Shareholder; Spouse/Partner; Phase V Technologies, Inc. G.M. Steil: Consultant; Self; Eli Lilly and Company, Profusa, Inc. D.S. Ludwig: Other Relationship; Self; Various publishers. Funding National Institute of Diabetes and Digestive and Kidney Diseases (K12DK094721, K24DK082730)