British journal of hospital medicine (London, England : 2005) · 2026
The Dawn Phenomenon Exacerbates Post-Breakfast Hyperglycemia in Type 2 Diabetes Mellitus: A Cross-Sectional Continuous Glucose Monitoring Study.
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Tan Wen, Zhang Jing, Jiang Cuiping, Huang Yuxin, Tao Xiaoming
Аннотация
AIMS/BACKGROUND: The dawn phenomenon (DP), characterized by spontaneous morning hyperglycemia in type 2 diabetes mellitus (T2DM), may exacerbate post-breakfast glucose excursions. This study investigated the association between DP and postprandial hyperglycemia, referred to as the "extended dawn phenomenon".
METHODS: In this cross-sectional study, 500 T2DM patients (glycated hemoglobin A1c (HbA1c) <7.5%) were recruited from Huadong Hospital, Fudan University between 2021 and 2023. A total of 40 participants were excluded due to incomplete data, resulting in 460 patients for final analysis. All participants underwent continuous glucose monitoring (CGM) and were stratified by the magnitude of DP (δDawn, defined as the difference between fasting glucose and nocturnal nadir glucose, with a threshold of ≥1.11 mmol/L). They were then matched by fasting glucose. Glycemic profiles, including peak post-breakfast glucose and time-in-range (TIR; percentage of time within the target glucose range of 3.9-10.0 mmol/L), were compared between groups. Multivariable logistic regression was used to identify determinants of post-breakfast hyperglycemia.
RESULTS: Despite comparable fasting glucose levels, patients with DP exhibited higher peak post-breakfast glucose (median (interquartile ranges [IQR]): 9.7 [8.2-10.7] vs 8.9 [8.0-10.0] mmol/L, p = 0.02) and reduced TIR in the overall cohort (94.1% [85.8-100.0] vs 100.0% [92.3-100.0], p < 0.001), although this difference attenuated after matching (p = 0.133). δDawn independently predicted post-breakfast hyperglycemia (odds ratio (OR) = 1.591, 95% confidence interval (CI): 1.283-1.993, p < 0.001), along with HbA1c (OR = 2.322, 95% CI: 1.530-3.566, p < 0.001), homeostatic model assessment for insulin resistance (HOMA-IR) (OR = 1.308, 95% CI: 1.110-1.548, p = 0.001), and homeostasis model assessment of β-cell function (HOMA-β) (OR = 0.990, 95% CI: 0.983-0.997, p = 0.004).
CONCLUSION: DP contributes to prolonged postprandial hyperglycemia, underscoring its role as a potential therapeutic target for optimizing glycemic control in T2DM.
METHODS: In this cross-sectional study, 500 T2DM patients (glycated hemoglobin A1c (HbA1c) <7.5%) were recruited from Huadong Hospital, Fudan University between 2021 and 2023. A total of 40 participants were excluded due to incomplete data, resulting in 460 patients for final analysis. All participants underwent continuous glucose monitoring (CGM) and were stratified by the magnitude of DP (δDawn, defined as the difference between fasting glucose and nocturnal nadir glucose, with a threshold of ≥1.11 mmol/L). They were then matched by fasting glucose. Glycemic profiles, including peak post-breakfast glucose and time-in-range (TIR; percentage of time within the target glucose range of 3.9-10.0 mmol/L), were compared between groups. Multivariable logistic regression was used to identify determinants of post-breakfast hyperglycemia.
RESULTS: Despite comparable fasting glucose levels, patients with DP exhibited higher peak post-breakfast glucose (median (interquartile ranges [IQR]): 9.7 [8.2-10.7] vs 8.9 [8.0-10.0] mmol/L, p = 0.02) and reduced TIR in the overall cohort (94.1% [85.8-100.0] vs 100.0% [92.3-100.0], p < 0.001), although this difference attenuated after matching (p = 0.133). δDawn independently predicted post-breakfast hyperglycemia (odds ratio (OR) = 1.591, 95% confidence interval (CI): 1.283-1.993, p < 0.001), along with HbA1c (OR = 2.322, 95% CI: 1.530-3.566, p < 0.001), homeostatic model assessment for insulin resistance (HOMA-IR) (OR = 1.308, 95% CI: 1.110-1.548, p = 0.001), and homeostasis model assessment of β-cell function (HOMA-β) (OR = 0.990, 95% CI: 0.983-0.997, p = 0.004).
CONCLUSION: DP contributes to prolonged postprandial hyperglycemia, underscoring its role as a potential therapeutic target for optimizing glycemic control in T2DM.