Delayed gastric emptying in the obese: an assessment using the non‐invasive ¹³C‐octanoic acid breath test

Abstract

The present study demonstrated a prolonged lag phase and delayed gastric emptying in obese women when compared to lean women. This delay may be as a consequence of high-fat diets, a sedentary lifestyle and increased gastric distension associated with obesity, or a contributing factor in the pathogenesis of obesity resulting from the inactivation of gastrointestinal satiety signals and in an increase in food intake.

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

“…Our evidence for inbred strain differences in gastric emptying rate extends the observations of Kirby et al (24) and provides new information on the identity of candidate genes contributing to this phenotype. Our results are similar in magnitude to those observed between lean and obese humans (13%) (22) and are consistent with the effects of known GLP-1 receptor agonists on food intake and gastric emptying (51). The modest effect size on gastric emptying rate in our study is consistent with the typical size of individual genetic contributions to polygenic traits.…”

Postgraduate Symposium The role of fat in gastric emptying and satiety: acute and chronic effects

“…A delayed lag time has also been observed (55)(56)(57)(58) . It has been postulated that disordered GE is not a major factor in the pathogenesis of obesity but secondary to weight gain and may be related to increased gallbladder volume and reduced postprandial gallbladder emptying in obese patients (57) .…”

“…It has also been reported in the literature that GE times are longer in the obese population for solid food (55)(56)(57)(58) and for liquids (55,57) . A delayed lag time has also been observed (55)(56)(57)(58) .…”

“…GE of liquid is therefore unaffected, as liquification is not necessary and hence GE occurs at the same rate in obese and normal-weight individuals. A further theory that supports delayed GE is that it may actually contribute to obesity rather than be a consequence of obesity (58) . A lack of nutrients in the duodenum resulting from reduced GE means that GI hormones responsible for the regulation of both GE and satiety are not released in high enough concentrations.…”

“…It has been postulated that disordered GE is not a major factor in the pathogenesis of obesity but secondary to weight gain and may be related to increased gallbladder volume and reduced postprandial gallbladder emptying in obese patients (57) . It has also been suggested that the delay in GE can be attributed to slower distribution of the meal as a result of a reduction in fundal tone, altered sensitivity of the stretch receptors or a change in antral area and mixing (58) . These changes may be a consequence of increased gastric distension and HF diets.…”