The acute effect of D-allulose consumption on postprandial glycaemia and insulin secretion in healthy individuals

In 2015, Public Health England challenged the food industry to reduce the free-sugars content of their sweetened products by 2020. However, whilst there has been some success in reformulating sugar-sweetened beverages, breakfast cereals and dairy products to reduce their sugars content, the contribution of sucrose to the taste and texture of sweetened baked goods and confectionery has been difficult to replace using readily available non-nutritive sweeteners (1) . D-allulose, a C3-epimer of fructose with low available energy content (2) and similar physicochemical properties to sucrose, is a candidate for replacing sucrose and glucose in sweetened foods to reduce energy content and glycaemic load. However, the incorporation of D-allulose into sweetened high- carbohydrate food products could confer additional health benefits. In vitro , D-allulose appears to compete with glucose at GLUT2 on the enterocyte basolateral membrane (3) (slowing glucose permeation) and stimulate glucokinase translocation; increasing glycogen synthesis in hepatocytes (4) and insulin secretion in β- cells (5) , with postprandial glycaemia being attenuated in humans after D-allulose consumption in a drink alongside foods and drinks containing glucose (6) . However, there is limited information concerning glucose profile and insulin secretion when D-allulose is integrated into consumed foods. The study aimed to investigate the effects of D-allulose consumption (within a high-carbohydrate breakfast) on glycaemia, insulinaemia and C- peptide concentration in healthy adults. This randomised, double-blinded, placebo-controlled, crossover study investigated the effects of D-allulose consumption (within a high-carbohydrate breakfast) on postprandial BG, serum insulin and C-peptide concentrations in twelve healthy young (19-26y), non- obese adults (6M:6F). A high glycaemic index porridge, sweetened with 10g glucose and either 15g of D-allulose or 0.06g sodium saccharin (matched-sweetness control), were consumed across two visits. BG, insulin and C-peptide were measured when fasted and at timepoints across 180 minutes following test meals. Single measurements were compared between visits using paired students t-test or Wilcoxon signed rank test, with comparisons in variables measured at more than one timepoint carried out using 2-way ANOVA with repeated measures. Peak concentration, the postprandial incremental response and net incremental area- under-curves (iAUC180) across 180-minutes for BG and insulin did not differ between meals.However, incremental BG response differed in the second half of the measurement period (Time x Meal: P<0.001; ηp 2 = 0.386), with this variable being lower at 90min (Control: 057 ± 0.59 mmol.l -1 , D-allulose: 0.12 ± 0.57 mmol.l -1 ) and 105min (Control: 0.54 ± 0.68 mmol.l -1 , D- allulose: -0.02 ± 0.47 mmol.l -1 ) after D-allulose consumption (both P<0.05). Moreover, C-peptide iAUC180 was lower after D-allulose consumption (Control: 135 ± 62 nmol. l-1.180min, D-allulose: 83 ± 24 nmol.l -1 .180min; P<0.05). In young, healthy individuals, the addition of D-allulose to a standardised porridge breakfast reduced BG in the late postprandial period, but did not suppress the initial hyperglycaemic response to eating. Moreover, D-allulose consumption did not enhance insulin secretion, as described in vitro .