Participants with relatively well-controlled type 2 diabetes (T2D) experience an increased rate of gastric emptying compared with healthy controls, according to study results published in The Journal of Clinical Endocrinology & Metabolism.
Glucagon-like peptide 1 receptor agonists slow the speed of gastric emptying and are most effective in reducing postprandial glycemia in individuals with rapid gastric emptying. Therefore, baseline rate of gastric emptying may be a key determinant in response to therapy. In this study, researchers evaluated the rate of gastric emptying in community-based participants with controlled T2D, healthy older controls, and healthy younger controls. Participants with controlled T2D were diagnosed according to American Diabetes Association criteria, had a glycated hemoglobin (HbA1c) level ≥6.0% and ≤7.9%, and managed their diabetes through diet or metformin monotherapy.
Gastric emptying was measured by a CO₂ breath test and blood glucose concentrations were measured using a glucometer. A subset of participants also completed an upper gastrointestinal symptom questionnaire. Baseline measurements were completed before the participants ate a standard mashed potato-based meal. Breath samples were collected at 5-minute intervals for the first hour after the meal and 15-minute intervals for the next 3 hours. Blood samples were collected at 15 minutes, 30 minutes, 1 hour, 1.5 hours, 2 hours, 3 hours, and 4 hours after meal consumption.
Of 111 participants with controlled T2D included in this study, 71 were men, mean age was 64.8 years, mean body mass index was 29.7 kg/m², and mean HbA1c was 6.6%. There were 18 healthy older controls (mean age, 65.4 years) and 15 healthy younger controls (mean age, 21.3 years) included in the study.
When comparing the 2 control cohorts, the younger cohort had a mean gastric emptying time of 3.0 kcal/min, while the older cohort had a mean gastric emptying time of 2.3 kcal/min (P =.0008). Peak blood glucose occurred approximately 30 minutes after eating in the younger cohort and at approximately 60 minutes in the older cohort (group effect, P <.001; group by time interaction, P <.0001).
Changes in increments of postprandial HbA1c were closely related to rate of gastric emptying in participants with T2D. When comparing the cohort with controlled T2D and the healthy older controls cohort, the participants with T2D had a significantly faster mean gastric emptying rate at 2.8 kcal/min (P =.0005) and had significantly higher blood glucose concentrations at all time points (P <.05).
When comparing participants who managed their diabetes with diet vs metformin, participants using diet had a mean gastric emptying rate of 2.7 kcal/min, while participants using metformin had a mean gastric emptying rate of 3.0 kcal/min (P =.011). Blood glucose concentrations were also lower in participants managing diabetes with diet alone (group effect, P =.007; group by time interaction, P =.01).
Prevalence of gastrointestinal symptoms was comparable in the subset of patients with T2D who completed the questionnaire and participants in the older control cohort.
Limitations to this study include the small size of the control cohort, the majority of the participants in the healthy older cohort having impaired fasting glucose, and not having the ability to control previous dietary habits.
The researchers concluded their findings are “of high clinical relevance, because the subset of patients with relatively good [glycemic] control (HbA1c <7.9%) is most likely to benefit from interventions that target postprandial [glycemia]. Evaluation of gastric emptying at baseline, such as using a point-of-care 13C-octaonoic breath test, may potentially [individualize] therapy in [T2D].”
Several authors reported associations with pharmaceutical companies. Please refer to original reference for a complete list of authors’ disclosures.
Watson LE, Xie C, Wang X, et al. Gastric emptying in patients with well-controlled type 2 diabetes compared to non-diabetic young and older controls [published online April 1, 2019]. J Clin Endocrinol Metab. doi:10.1210/jc.2018-02736