Metabolic and Hormonal Responses to Isomaltulose Ingestion Before or During Sustained Submaximal Exercise in Adults with Type 1 Diabetes Using Automated Insulin Delivery Systems.

OBJECTIVES

This article compares metabolic, pancreatic, and gut-derived hormone responses to isomaltulose ingestion, before versus during submaximal sustained exercise, in adults with type 1 diabetes (T1D) using automated insulin delivery systems.

METHODS

In a randomized, cross-over trial, eight participants with T1D being treated with automated insulin pumps (five females, age: 47 ± 16 years, BMI: 27.5 ± 3.8 kg·m, diabetes duration: 23 ± 11 years, HbA1c: 8.3 ± 0.9 [67.5 ± 9.5]% [mmol/mol]) attended the laboratory on two separate occasions and consumed an isocaloric amount of isomaltulose as either (1) a single serving (0.75g CHO·kg BM) with a 25% reduction in bolus insulin 90 min before 45 min of cycling (PEC) or (2) three separate isocaloric servings (0.25g CHO·kg BM each) without bolus insulin during exercise (DEC). Plasma glucose (PG), gut incretins (GLP-1 and GIP), pancreatic glucagon, exogenous insulin, and whole-body fuel oxidation rates were determined. Data were treated via a two-way repeated measures ANOVA, with ≤ 0.05 accepted as significant.

RESULTS

PG concentrations throughout exercise were higher and less variable with DEC compared to PEC. The exercise-induced change in PG was directionally divergent between trials (PEC: ∆ - 3.2 ± 1.2 mmol/L vs. DEC: ∆ + 1.7 ± 1.5 mmol/L, < 0.001), changing at a rate of -0.07 ± 0.03 mmol/L/min with PEC and +0.04 ± 0.03 mmol/L/min with DEC ( < 0.001 between conditions). Throughout the exercise period, GLP-1, GIP, glucagon, and total insulin concentrations were lower with DEC (all ≤ 0.02). The oxidation rates of carbohydrates were lower ( = 0.009) and of lipids were greater ( = 0.014) with DEC compared to PEC.

CONCLUSIONS

The consumption of smaller servings of isomaltulose during, rather than as a single isocaloric serving before, submaximal sustained exercise provided (i) a better glycemic protective effect, (ii) a lesser push on pancreatic and gut-mediated glucoregulatory hormones, and (iii) a lower reliance on whole-body carbohydrate oxidation. Such information serves to remind us of the potential importance of nutrition for modulating the metabolic fate of an acute bout of exercise and may help inform best practice guidelines for exercise management in the T1D-sphere.