Increased nutrient sensitivity and plasma concentrations of enteral hormones during duodenal nutrient infusion in functional dyspepsia.
OBJECTIVE
Functional dyspepsia is predominantly attributed to gastric sensorimotor dysfunctions. The contribution of intestinal chemosensitivity to symptoms is not understood. We evaluated symptoms and plasma hormones during enteral nutrient infusion and the association with impaired glucose tolerance and quality-of-life (QOL) scores in patients with functional dyspepsia vs. healthy controls.


METHODS
Enteral hormonal responses and symptoms were measured during isocaloric and isovolumic dextrose and lipid infusions into the duodenum in 30 patients with functional dyspepsia (n=27) or nausea and vomiting (n=3) and 35 healthy controls. Infusions were administered in randomized order over 120 min each, with a 120-min washout. Cholecystokinin, glucose-dependent insulinotropic peptide, glucagon-like peptide 1 (GLP1), and peptide YY were measured during infusions.


RESULTS
Moderate or more severe symptoms during lipid (4 controls vs. 14 patients) and dextrose (1 control vs. 12 patients) infusions were more prevalent in patients than controls (P≤0.01), associated with higher dyspepsia symptom score (P=0.01), worse QOL (P=0.01), and greater plasma hormone concentrations (e.g., GLP1 during lipid infusion). Moderate or more severe symptoms during enteral infusion explained 18%, and depression score explained 21%, of interpatient variation in QOL. Eight patients had impaired glucose tolerance, associated with greater plasma GLP1 and peptide YY concentrations during dextrose and lipid infusions, respectively.


CONCLUSIONS
Increased sensitivity to enteral dextrose and lipid infusions was associated with greater plasma enteral hormone concentrations, more severe daily symptoms, and worse QOL in functional dyspepsia. These observations are consistent with the hypothesis that enteral hormones mediate increased intestinal sensitivity to nutrients in functional dyspepsia.
Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Adil E
AE
Bharucha
Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Michael
M
Camilleri
Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Duane D
DD
Burton
Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Shannon L
SL
Thieke
Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Kelly J
KJ
Feuerhak
Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic, Rochester, Minnesota, USA.
Ananda
A
Basu
Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota, USA.
Alan R
AR
Zinsmeister
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D002096:C-Peptide / Q000097:blood; D016022:Case-Control Studies; D002766:Cholecystokinin / Q000097:blood; D004386:Duodenum / Q000378:metabolism*; D004415:Dyspepsia / Q000097:blood / Q000378:metabolism*; D004750:Enteral Nutrition; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D054439:Ghrelin / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D005947:Glucose; D018149:Glucose Intolerance / Q000097:blood / Q000378:metabolism*; D006801:Humans; D008055:Lipids; D008297:Male; D019894:Peptide YY / Q000097:blood; D011788:Quality of Life; D012720:Severity of Illness Index
D001786:Blood Glucose; D002096:C-Peptide; D054439:Ghrelin; D008055:Lipids; D019894:Peptide YY; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1; D002766:Cholecystokinin; D005947:Glucose