Gastric emptying (GE) significantly influences postprandial glycemia in both healthy individuals and those with type 2 diabetes (T2D). Even small variations in GE rate can substantially affect postprandial blood glucose, especially in T2D due to impaired glucose tolerance. Interventions that slow GE, such as nutrient preloads or GLP-1 receptor agonists (GLP-1RAs), reduce postprandial glycemia, while GE acceleration increases it. The rate of GE in T2D also predicts the effectiveness of glucose-lowering therapies like GLP-1RAs and DPP-4 inhibitors. In healthy individuals, GE occurs at a relatively constant rate, but in T2D, this rate is highly variable between individuals, although it remains reasonably reproducible within the same individual using the same test meal. However, it's unclear whether GE assessed with a standard test meal, such as a 75g oral glucose drink, predicts the glycemic response to other meals. This study aimed to determine (i) the correlation between glycemic responses to a glucose drink and mixed meals with GE of a 75g glucose drink, and (ii) the relationship between GE of a glucose drink and antecedent glycemic control in T2D.

Existing research demonstrates GE's crucial role in postprandial glycemic response in both health and diabetes. Studies show that slowing GE through dietary or pharmacological interventions reduces postprandial glucose excursions in T2D. Conversely, accelerating GE increases these excursions. The predictability of postprandial glucose-lowering responses to specific therapies, such as GLP-1RAs and DPP-4 inhibitors, is also linked to the baseline GE rate. While individual GE rates are relatively consistent, the relationship between GE measured using a standard test meal (like a 75g glucose drink) and the glycemic response to more physiological meals remains uncertain. Understanding this is crucial for choosing appropriate test meals and managing postprandial glycemia. Current glycemic load and index recommendations lack a strong mechanistic basis related to nutrient delivery rates.

This prospective study enrolled 55 treatment-naive Chinese adults with newly diagnosed T2D. Participants were admitted to a clinical research unit for three consecutive days. On Day 1, a medical history was obtained, and a continuous glucose monitoring (CGM) sensor was inserted. On Day 2, participants consumed three standardized meals (breakfast, lunch, and dinner) with continuous glucose monitoring. On Day 3, after an overnight fast, participants ingested a 75g glucose drink containing 13C-acetate to assess GE (breath test) and plasma glucose response. Breath samples were collected every 15 minutes for 3 hours, and venous blood samples were collected at various time points to measure plasma glucose, HbA1c, and serum fructosamine. The gastric half-emptying time (T50) was calculated using the Wagner-Nelson method. Statistical analyses included univariate linear regression to assess correlations between glycemic responses (incremental area under the curve, iAUC) to the glucose drink and mixed meals with the T50 of the glucose drink, and between GE (T50) and markers of short-, medium-, and long-term glycemic control (fasting plasma glucose (FPG), 24-hour mean interstitial glucose, serum fructosamine, HbA1c).

The study included 55 newly diagnosed, treatment-naive participants with T2D. The 24-hour mean interstitial glucose was 13.4 ± 0.3 mmol/L, reflecting suboptimal glycemic control. Following the 75g glucose drink, plasma glucose peaked at 22.1 ± 0.4 mmol/L at 90 minutes. The T50 of the glucose drink ranged from 26.0 to 134.7 minutes (mean 73.5 ± 3.3 min). Plasma glucose iAUCs within 2 hours after the oral glucose load were inversely related to T50 (r = -0.34, P = 0.012). Similarly, interstitial glucose iAUCs within 2 hours after breakfast (r = -0.34, P = 0.012) and dinner (r = -0.28, P = 0.040) were inversely related to the oral glucose T50. Importantly, the T50 was not significantly related to FPG, 24-hour mean interstitial glucose, serum fructosamine, or HbA1c, indicating no influence of antecedent glycemic control on GE.

This study demonstrates that in newly diagnosed, treatment-naive individuals with T2D, GE of a 75g glucose drink accurately predicts the glycemic response to both a glucose drink and mixed meals, particularly breakfast and dinner. This finding supports the use of a 75g glucose drink as a suitable test meal for measuring GE in this population. The lack of correlation between GE and antecedent glycemic markers suggests that spontaneous short-, medium-, or long-term hyperglycemia does not substantially impact GE. This contrasts with studies showing that abrupt glucose increases can slow GE. The consistency of GE within individuals, regardless of overall glycemic control, emphasizes its role in postprandial glycemic excursions and the potential to use interventions targeting GE to manage T2D.

This study confirms that gastric emptying (GE) of a 75g glucose drink is a strong predictor of glycemic response to various meals in newly diagnosed, treatment-naive individuals with T2D, independent of pre-existing glycemic levels. This supports the use of a standardized glucose drink test to assess GE and its relevance to managing postprandial hyperglycemia. Future research should investigate the impact of different glucose-lowering therapies and varying degrees of glycemic control on the relationship between GE and glycemic response.

The study's relatively small sample size and focus on treatment-naive individuals may limit generalizability to the broader T2D population. The observational nature of the study prevents causal conclusions about the relationship between GE and antecedent glycemic control. The lack of detailed dietary information may have introduced some variability.