2025年12月18日出版的《细胞—代谢》杂志发表了马斯特里赫特大学Joris Hoeks小组的最新成果，他们发现了办公时间的自然光可以改善葡萄糖控制和全身底物代谢。

由于人体80%-90%的时间是在室内度过的，而日光是中央生物钟的主要同步器，因此长期缺乏日光越来越被认为是代谢性疾病（如2型糖尿病）的危险因素。在一项随机交叉设计（NCT05263232）中，13名2型糖尿病患者在连续4.5天的办公时间内暴露在通过窗户的自然光下，而不是恒定的人工照明下。持续的血糖监测显示，参与者在正常血糖范围内的时间更长，全身底物代谢在白天转向更依赖脂肪氧化。骨骼肌活检培养的原代肌管在日光照射后表现出相提前。多组学分析揭示了日光诱导的血清代谢物、脂质和单核细胞转录物的差异。他们的研究结果表明，自然光照射对2型糖尿病患者的代谢有积极的影响，可以支持代谢疾病的治疗。

附：英文原文

Title: Natural daylight during office hours improves glucose control and whole-body substrate metabolism

Author: Jan-Frieder Harmsen, Ivo Habets, Andrew D. Biancolin, Agata Lesniewska, Nicholas E. Phillips, Loic Metz, Juan Sanchez-Avila, Marit Kotte, Merel Timmermans, Dzhansel Hashim, Soraya S. de Kam, Gert Schaart, Johanna A. Jrgensen, Anne Gemmink, Esther Moonen-Kornips, Daniel Doligkeit, Tineke van de Weijer, Mijke Buitinga, Florian Haans, Rebecca De Lorenzo, Hannah Pallubinsky, Marijke C.M. Gordijn, Tinh-Hai Collet, Achim Kramer, Patrick Schrauwen, Charna Dibner, Joris Hoeks

Issue&Volume: 2025-12-18

Abstract: Because 80%–90% of our time is spent indoors and daylight is the main synchronizer of the central biological clock, the chronic lack of daylight is increasingly considered as a risk factor for metabolic diseases, such as type 2 diabetes. In a randomized crossover design (NCT05263232), 13 individuals with type 2 diabetes were exposed to natural daylight facilitated through windows vs. constant artificial lighting during office hours for 4.5 consecutive days. Continuous glucose monitoring revealed that participants spent more time in the normal glucose range, and whole-body substrate metabolism shifted toward a greater reliance on fat oxidation during daylight. Primary myotubes cultured from skeletal muscle biopsies displayed a phase advance after daylight exposure. Multi-omic analyses revealed daylight-induced differences in serum metabolites, lipids, and monocyte transcripts. Our findings suggest that natural daylight exposure has a positive metabolic impact on individuals with type 2 diabetes and could support the treatment of metabolic diseases.

DOI: 10.1016/j.cmet.2025.11.006

Source: https://www.cell.com/cell-metabolism/abstract/S1550-4131(25)00490-5