OBJECTIVE The circadian clock regulates glucose metabolism by mediating the activity of metabolic enzymes, hormones, and transport systems. Breakfast skipping and night eating have been associated with high HbA_1c and postprandial hyperglycemia after lunch and dinner. Our aim was to explore the acute effect of breakfast consumption or omission on glucose homeostasis and clock gene expression in healthy individuals and individuals with type 2 diabetes.

RESEARCH DESIGN AND METHODS In a cross-over design, 18 healthy volunteers and 18 volunteers with 14.5 ± 1.5 years diabetes, BMI 30.7 ± 1.1 kg/m², and HbA_1c 7.6 ± 0.1% (59.6 ± 0.8 mmol/mol) were randomly assigned to a test day with breakfast and lunch (YesB) and a test day with only lunch (NoB). Postprandial clock and clock-controlled gene expression, plasma glucose, insulin, intact glucagon-like peptide-1 (iGLP-1), and dipeptidyl peptidase IV (DPP-IV) plasma activity were assessed after breakfast and lunch.

RESULTS In healthy individuals, the expression level of Per1, Cry1, Rorα, and Sirt1 was lower (P < 0.05) but Clock was higher (P < 0.05) after breakfast. In contrast, in individuals with type 2 diabetes, Per1, Per2, and Sirt1 only slightly, but significantly, decreased and Rorα increased (P < 0.05) after breakfast. In healthy individuals, the expression level of Bmal1, Rorα, and Sirt1 was higher (P < 0.05) after lunch on YesB day, whereas the other clock genes remained unchanged. In individuals with type 2 diabetes, Bmal1, Per1, Per2, Rev-erbα, and Ampk increased (P < 0.05) after lunch on the YesB day. Omission of breakfast altered clock and metabolic gene expression in both healthy and individuals with type 2 diabetes.

CONCLUSIONS Breakfast consumption acutely affects clock and clock-controlled gene expression leading to normal oscillation. Breakfast skipping adversely affects clock and clock-controlled gene expression and is correlated with increased postprandial glycemic response in both healthy individuals and individuals with diabetes.

目的生物钟通过介导代谢酶、激素和运输系统的活动来调节葡萄糖代谢。不吃早餐和夜间进食与午餐和晚餐后高 HbA _1c以及餐后高血糖有关。我们的目的是探讨健康个体和 2 型糖尿病患者吃或不吃早餐对葡萄糖稳态和时钟基因表达的急性影响。

研究设计和方法在交叉设计中，18 名健康志愿者和 18 名患有 14.5 ± 1.5 年糖尿病、BMI 30.7 ± 1.1 kg/m ²和 HbA _1c 7.6 ± 0.1% (59.6 ± 0.8 mmol/mol) 的志愿者被随机分组分配到包含早餐和午餐的测试日 (YesB) 和仅包含午餐的测试日 (NoB)。早餐和午餐后评估餐后时钟和时钟控制基因表达、血浆葡萄糖、胰岛素、完整胰高血糖素样肽-1 (iGLP-1) 和二肽基肽酶 IV (DPP-IV) 血浆活性。

结果健康个体早餐后Per1 、 Cry1 、 Rorα 、 Sirt1表达量较低（ P <0.05）， Clock表达量较高（ P <0.05）。相比之下，在 2 型糖尿病患者中，早餐后Per1 、 Per2和Sirt1仅轻微但显着下降，而Rorα 则增加 ( P < 0.05)。在健康个体中，YesB 日午餐后Bmal1 、 Rorα和Sirt1的表达水平较高（ P < 0.05），而其他时钟基因则保持不变。在 2 型糖尿病患者中，YesB 日午餐后， Bmal1 、 Per1 、 Per2 、 Rev-erbα和Ampk增加 ( P < 0.05)。不吃早餐会改变健康人和 2 型糖尿病患者的生物钟和代谢基因表达。

结论吃早餐会严重影响生物钟和生物钟控制的基因表达，从而导致正常振荡。不吃早餐会对生物钟和生物钟控制的基因表达产生不利影响，并且与健康个体和糖尿病患者的餐后血糖反应增加相关。