Diabetes Unit, Wolfson Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Holon, Israel
Diabetes Unit, Wolfson Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Holon, Israel.
Diabetes Care. 2017 Nov;40(11):1573-1579. doi: 10.2337/dc16-2753. Epub 2017 Aug 22.
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 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.
In a crossover design, 18 healthy volunteers and 18 volunteers with 14.5 ± 1.5 years diabetes, BMI 30.7 ± 1.1 kg/m, and HbA 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.
In healthy individuals, the expression level of , , , and was lower ( < 0.05) but was higher ( < 0.05) after breakfast. In contrast, in individuals with type 2 diabetes, , , and only slightly, but significantly, decreased and increased ( < 0.05) after breakfast. In healthy individuals, the expression level of , , and was higher ( < 0.05) after lunch on YesB day, whereas the other clock genes remained unchanged. In individuals with type 2 diabetes, , , , , and increased ( < 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.
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.
生物钟通过调节代谢酶、激素和转运系统的活性来调节葡萄糖代谢。不吃早餐和夜间进食与 HbA 升高以及午餐和晚餐后餐后高血糖有关。我们的目的是探讨健康个体和 2 型糖尿病个体中早餐摄入或不摄入对葡萄糖稳态和时钟基因表达的急性影响。
在一项交叉设计中,将 18 名健康志愿者和 18 名糖尿病患者(糖尿病病程 14.5 ± 1.5 年,BMI 30.7 ± 1.1 kg/m2,HbA 7.6 ± 0.1%[59.6 ± 0.8 mmol/mol])随机分为早餐和午餐(YesB)日和仅午餐(NoB)日。分别在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)的血浆活性。
在健康个体中, 、 、 、 和 ( < 0.05)的表达水平较低,但 ( < 0.05)的表达水平较高。相反,在 2 型糖尿病患者中, 、 、 和 仅略有下降,但显著下降( < 0.05),而 则有所增加( < 0.05)。在健康个体中,YesB 日午餐后 、 、 和 ( < 0.05)的表达水平较高,而其他时钟基因保持不变。在 2 型糖尿病患者中,YesB 日午餐后 、 、 、 、 和 ( < 0.05)的表达水平升高。在健康个体和 2 型糖尿病患者中,不吃早餐会改变时钟和代谢基因的表达。
早餐摄入会急性影响时钟和时钟控制基因的表达,导致正常的波动。不吃早餐会对时钟和时钟控制基因的表达产生不利影响,并与健康个体和糖尿病个体的餐后血糖反应增加相关。