Abstract
Postprandial hyperglycemia (PPHG) is strongly linked with the future development of cardiovascular complications in type 2 diabetes (T2D). Hence, reducing postprandial glycemic excursions is essential in T2D treatment to slow progressive deficiency of β-cell function and prevent cardiovascular complications. Most of the metabolic processes involved in PPHG, i.e., β-cell secretory function, GLP-1 secretion, insulin sensitivity, muscular glucose uptake, and hepatic glucose production, are controlled by the circadian clock and display daily oscillation. Consequently, postprandial glycemia displays diurnal variation with a higher glycemic response after meals with the same carbohydrate content, consumed at dusk compared to the morning. T2D and meal timing schedule not synchronized with the circadian clock (i.e., skipping breakfast) are associated with disrupted clock gene expression and is linked to PPHG. In contrast, greater intake in the morning (i.e., high energy breakfast) than in the evening has a resetting effect on clock gene oscillations and beneficial effects on weight loss, appetite, and reduction of PPHG, independently of total energy intake. Therefore, resetting clock gene expression through a diet intervention consisting of meal timing aligned to the circadian clock, i.e., shifting most calories and carbohydrates to the early hours of the day, is a promising therapeutic approach to improve PPHG in T2D. This review will focus on recent studies, showing how a high-energy breakfast diet (Bdiet) has resetting and synchronizing actions on circadian clock genes expression, improving glucose metabolism, postprandial glycemic excursions along with weight loss in T2D.
Highlights
Postprandial hyperglycemia (PPHG) in type 2 diabetes (T2D) strongly contributes to glycated hemoglobin (HbA1c) values [1]
In two crossover studies in T2D patients, we explored whether skipping breakfast in a single day (NoB) versus another day consuming high energy and CH breakfast (YesB) influences the clock gene expression and the PPHG after subsequent isocaloric meals. [43,56]
Postprandial hyperglycemia in T2D leads to a progressive decline of β-cell function and increases the cardiovascular risk in T2D [2,6,7]
Summary
Postprandial hyperglycemia (PPHG) in type 2 diabetes (T2D) strongly contributes to glycated hemoglobin (HbA1c) values [1]. With day/night cycle, often imposed in modern society, like shift workers, skipping breakfast, snacking all day, including in the evening hours, are associated with disrupted clock gene expression and linked with aberrant metabolic responses, weight gain, PPHG, increased risk for T2D [12,27,34,37,42,45,46,47,48,49,50,51,52], and cardiovascular complications [53]. Meal-timing pattern, aligned with the circadian clock, consuming high in energy breakfast, exerts a powerful effect on the clock network temporal synchronization, thereby improving the postprandial glycemic responses across the day in healthy and T2D patients [15,35,39,43,56]. In this review we discuss recent studies showing how the high energy breakfast diet designed as “big breakfast diet” (Bdiet) has resetting and synchronizing actions on clock gene expression, improving glucose metabolism, postprandial glycemic excursions, and bodyweight in T2D
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