期刊
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
卷 104, 期 6, 页码 1967-1977出版社
ENDOCRINE SOC
DOI: 10.1210/jc.2018-01623
关键词
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资金
- National Institute of Diabetes and Digestive and Kidney Diseases Grant [DK68055]
- US Public Health Service National Institutes of Health [R01 DK68055]
- National Center for Advancing Translational Sciences [UL1TR000135]
Context: Delayed gastric emptying (GE) is common but often asymptomatic in diabetes. The relationship between symptoms, glycemia, and neurohormonal functions, including glucagonlike peptide 1 (GLP-1), are unclear. Objectives: To assess whether GE disturbances, symptoms during a GE study, and symptoms during enteral lipid infusion explain daily symptoms and whether GLP-1 mediates symptoms during enteral lipid infusion. Design: In this randomized controlled trial, GE, enteral lipid infusion, gastrointestinal (GI) symptoms during these assessments, autonomic functions, glycosylated hemoglobin (HbA1c), and daily GI symptoms (2-week Gastroparesis Cardinal Symptom Index diary) were evaluated. During enteral lipid infusion, participants received the GLP-1 antagonist exendin 9-39 or placebo. Setting: Single tertiary referral center. Participants: 24 healthy controls and 40 patients with diabetic gastroenteropathy. Main Outcome Measures: GE, symptoms during enteral lipid infusion, and the effect of exendin 939 on the latter. Results: In patients, GE was normal (55%), delayed (33%), or rapid (12%). During lipid infusion, GI symptoms tended to be greater (P = 0.06) in patients with diabetes mellitus (DM) than controls; exendin 9-39 did not affect symptoms. The HbA1c was inversely correlated with the mean symptom score during the GE study (r = -0.46, P = 0.003) and lipid infusion (r = -0.47, P < 0.01). GE and symptoms during GE study accounted for 40% and 32%, respectively, of the variance in daily symptom severity and quality of life. Conclusions: In DM gastroenteropathy, GE and symptoms during a GE study explain daily symptoms. Symptoms during enteral lipid infusion were borderline increased but not reduced by a GLP-1 antagonist.
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