Pivovarova Olga, Jürchott Karsten, Rudovich Natalia, Hornemann Silke, Ye Lu, Möckel Simona, Murahovschi Veronica, Kessler Katharina, Seltmann Anne-Cathrin, Maser-Gluth Christiane, Mazuch Jeannine, Kruse Michael, Busjahn Andreas, Kramer Achim, Pfeiffer Andreas F H
Department of Clinical Nutrition (O.P., N.R., S.H., Y.L., S.M., V.M., K.K., A.-C.S., M.K., A.F.H.P.), German Institute of Human Nutrition Potsdam-Rehbruecke, 14558 Nuthetal, Germany; Department of Endocrinology (O.P., N.R., Y.L., V.M., K.K., M.K., A.F.H.P.), Diabetes and Nutrition, Campus Benjamin Franklin, Charité University Medicine, 12203 Berlin, Germany; Berlin-Brandenburg Center for Regenerative Therapies (K.J.), Charité University Medicine, 13353 Berlin, Germany; Institute for Pharmacology (C.M.-G.), University of Heidelberg, 69120 Heidelberg, Germany; Laboratory of Chronobiology (J.M., A.K.), Institute for Medical Immunology, Charité University Medicine, 10115 Berlin, Germany; and HealthTwiSt GmbH (A.B.), 13125 Berlin, Germany.
J Clin Endocrinol Metab. 2015 Jun;100(6):2291-302. doi: 10.1210/jc.2014-3868. Epub 2015 Mar 30.
The circadian clock coordinates numerous metabolic processes with light-dark and feeding regimens. However, in humans it is unknown whether dietary patterns influence circadian rhythms.
We examined the effects of switching from a high-carbohydrate, low-fat diet to a low-carbohydrate, high fat (LC/HFD) isocaloric diet on the central and peripheral circadian clocks in humans.
Diurnal patterns of salivary cortisol and gene expression were analyzed in blood monocytes of 29 nonobese healthy subjects before and 1 and 6 weeks after the dietary switch. For this, we established a method of rhythm prediction by 3-time point data.
The centrally driven cortisol rhythm showed a phase delay 1 and 6 weeks after the dietary switch to a LC/HFD as well as an amplitude increase. The dietary switch altered diurnal oscillations of core clock genes (PER1, PER2, PER3, and TEF) and inflammatory genes (CD14, CD180, NFKBIA, and IL1B). The LC/HFD also affected the expression of nonoscillating genes contributing to energy metabolism (SIRT1) and fat metabolism (ACOX3 and IDH3A). Expression of clock genes but not of salivary cortisol in monocytes tightly correlated with levels of blood lipids and with expression of metabolic and inflammatory genes.
Our results suggest that the modulation of the dietary fat and carbohydrate content alters the function of the central and peripheral circadian clocks in humans.
昼夜节律钟将众多代谢过程与明暗周期和进食模式协调起来。然而，在人类中，饮食模式是否会影响昼夜节律尚不清楚。
我们研究了从高碳水化合物、低脂饮食转换为低碳水化合物、高脂肪（LC/HFD）等热量饮食对人类中枢和外周昼夜节律钟的影响。
在29名非肥胖健康受试者饮食转换前、转换后1周和6周，分析其血液单核细胞中唾液皮质醇的昼夜模式和基因表达。为此，我们建立了一种通过三个时间点数据进行节律预测的方法。
饮食转换为LC/HFD后1周和6周，中枢驱动的皮质醇节律出现相位延迟以及振幅增加。饮食转换改变了核心生物钟基因（PER1、PER2、PER3和TEF）和炎症基因（CD14、CD180、NFKBIA和IL1B）的昼夜振荡。LC/HFD还影响了参与能量代谢（SIRT1）和脂肪代谢（ACOX3和IDH3A）的非振荡基因的表达。单核细胞中生物钟基因的表达而非唾液皮质醇的表达与血脂水平以及代谢和炎症基因的表达密切相关。
我们的结果表明，饮食中脂肪和碳水化合物含量的调节会改变人类中枢和外周昼夜节律钟的功能。
