Abstract
This study aimed to examine gastric emptying rate and gastrointestinal hormone responses to fructose and glucose ingestion following 3 days of dietary fructose supplementation. Using the 13C-breath test method, gastric emptying rates of equicaloric fructose and glucose solutions were measured in 10 healthy men with prior fructose supplementation (fructose supplement, FS; glucose supplement, GS) and without prior fructose supplementation (fructose control, FC; glucose control, GC). In addition, circulating concentrations of acylated ghrelin (GHR), glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and insulin were determined, as well as leptin, lactate, and triglycerides. Increased dietary fructose ingestion resulted in accelerated gastric emptying rate of a fructose solution but not a glucose solution. No differences in GIP, GLP-1, or insulin incremental area under curve (iAUC) were found between control and supplement trials for either fructose or glucose ingestion. However, a trend for lower ghrelin iAUC was observed for FS compared to FC. In addition, a trend of lower GHR concentration was observed at 45 min for FS compared to FC and GHR concentration for GS was greater than GC at 10 min. The accelerated gastric emptying rate of fructose following short-term supplementation with fructose may be partially explained by subtle changes in delayed postprandial ghrelin suppression.
Highlights
Gastric emptying is a rate-limiting step in the delivery and absorption of nutrients and fluids in the small intestine
Participants reported to the laboratory on four occasions to complete four experimental trials; fructose with supplementation (FS), fructose with water control (FC), glucose with supplementation (GS) and glucose with water control (GC) as previously conducted by Yau et al [12]
Pre-ingestion urine osmolality (Table 1) was generally lower in each supplement trial compared to the control trials but was not statistically significant (p = 0.067)
Summary
Gastric emptying is a rate-limiting step in the delivery and absorption of nutrients and fluids in the small intestine. The rate at which nutrients empty from the stomach directly affects the period of gastric distension and nutrient sensing. Gastric distension causes both satiation and satiety [1]. A prolonged period of gastric distension due to delayed emptying may lead to a prolonged satiety period. A number of hormones secreted from the gastrointestinal tract involved in appetite regulation have been to shown to influence gastric emptying rate. The only orexigenic hormone, accelerates gastric emptying rate [2,3] whilst satiety hormones such as glucagon-like peptide-1 (GLP-1), peptide tyrosine tyrosine (PYY), and cholecystokinin (CCK) inhibit gastric emptying rate [4,5,6,7,8].
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