Literature DB >> 27880079

Relationship Between Gastric Emptying and Diurnal Glycemic Control in Type 1 Diabetes Mellitus: A Randomized Trial.

Gopanandan Parthasarathy1, Yogish C Kudva2, Phillip A Low3, Michael Camilleri1, Ananda Basu2, Adil E Bharucha1.   

Abstract

Context: In type 1 diabetes (T1D), delayed gastric emptying (GE) may predispose to a mismatch between insulin delivery and glucose absorption. Previous studies evaluated, only partly, the relationship between delayed GE and postprandial, but not diurnal, glycemia. Objective: To assess the relationship between GE disturbances and glycemic control in T1D and the effects of accelerating GE on glycemic control. Design, Setting, and Participants: This was a randomized placebo-controlled trial in 30 patients with T1D on an insulin pump at an academic medical center. Intervention(s): GE was evaluated with a [13C]-Spirulina breath test at baseline (GEbaseline), during intravenous saline or erythromycin (2 or 3 mg/kg; GEiv), and after 7 days of oral erythromycin or placebo (GEoral). Weighed meals were provided throughout the study. Main Outcome Measure(s): These were GE and continuous glucose monitoring (CGM).
Results: The baseline glycosylated hemoglobin was 7.6% ± 0.8% (60 ± 8.7 mmol/mol); 12 patients (40%) had delayed GE; faster GE was associated with a greater postprandial CGM-based glucose, but slower GE was not associated with postprandial hypoglycemia (<70 mg/dL). Intravenous (3 mg/kg) but not oral erythromycin accelerated GE. The relationship between GE and glycemia differed between the postprandial periods and the entire day. After adjusting for carbohydrate intake and insulin consumption, faster GE was associated with more hyperglycemia during the postprandial period but lower glucose values across the entire study. Conclusions: In T1D, pharmacologically mediated acceleration of GE increases postprandial CGM-based glucose. In contrast, delayed GE is associated with greater CGM-based glucose values over the entire day.
Copyright © 2017 by the Endocrine Society

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Year:  2017        PMID: 27880079      PMCID: PMC5413165          DOI: 10.1210/jc.2016-2809

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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