There is accumulating evidence for the benefit of a diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) for the management of irritable bowel syndrome symptoms. Whether FODMAPs alter the upper GI response to nutrients, including gastric accommodation, remains to be assessed. The objectives were to assess the role of different FODMAPs in the intragastric pressure response to nutrient ingestion (which reflects gastric accommodation), upper GI motility, meal-induced satiation and symptom generation.

A high resolution manometry and infusion catheter were positioned in the proximal stomach of healthy volunteers. After a stabilization period and when the subjects were in late phase II of the migrating motor complex, one of four solutions (fructans (38g/L), fructose (100g/L), FODMAP mix (80g/L) or glucose (100g/L) as control) were intragastrically infused at 60mL/min, three days to one week apart in a single-blind randomised cross-over order. The FODMAP mix consisted of 20g of fructans, 10g of galacto-oligosaccharides, sorbitol and mannitol and 30g of fructose dissolved in 1L of water. The infusion ended when subjects scored maximum satiation (0–5 scale). Intragastric pressure was recorded for the duration of the drink infusion and for the following 3hours. Intragastric pressure was presented as change from baseline (mean±SEM). Intensity of epigastric and GI symptoms were rated before the infusion, and then every 15minutes using a 100mm VAS. Results were compared using repeated measures ANOVA.

Twenty healthy volunteers (19–32y, 10 men, 18–44 BMI) were randomized. Two were smokers and none had GI symptoms or history of GI disease. Total ingested volumes at maximal satiation differed significantly between fructose and FODMAP mix (P=0.0197) (fructans 1383±193mL; fructose 1032±113mL, FODMAP mix 1302±129mL, glucose 1125±98mL). In all subjects and with each infusion, the intragastric pressure decreased initially to gradually recover thereafter. The mean intragastric pressure drop during infusion was significantly less for fructans (–2.25±0.15mmHg), when compared to all other solutions (fructose –3.21±0.26mmHg, P=0.0005; FODMAP mix –3.78±0.23mmHg, P<0.0001 and glucose –2.98±0.19mmHg, P=0.0113). Furthermore mean intragastric pressure differed significantly between FODMAP mix and glucose (P=0.0075). After recovery of the intragastric pressure drop, although all solutions remained constantly high in their pressure across the three hours post infusion, the fructans maintained a significantly higher intra-gastric pressure (3.7±0.19mmHg) compared to the fructose, FODMAP mix and glucose (2.7±0.19, 1.5±0.16 and 1.7±0.15mmHg, respectively) (P<0.0001). In comparison to the glucose, differences in symptoms were reported for wind following the fructans, fructose and FODMAP mix and for cramps following the fructose and FODMAP mix solutions (P<0.05).

This study indicates that fructans induce a significantly lower intragastric pressure response in the healthy state, when compared to the other FODMAPs and glucose. Unravelling the sensory, neural and/or hormonal pathways involved in the effect of fructans on gastric physiology require further mechanistic studies. The findings also offer opportunities to identify whether ingestion of fructans contribute to symptoms associated with impaired gastric accommodation seen in functional GI patients, including irritable bowel syndrome.