Cell Metabolism
Volume 34, Issue 10, 4 October 2022, Pages 1486-1498.e7
Journal home page for Cell Metabolism

Clinical and Translational Report
Late isocaloric eating increases hunger, decreases energy expenditure, and modifies metabolic pathways in adults with overweight and obesity

https://doi.org/10.1016/j.cmet.2022.09.007Get rights and content
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Highlights

  • Late eating increases waketime hunger and decreases 24-h serum leptin

  • Late eating decreases waketime energy expenditure and 24-h core body temperature

  • Late eating alters adipose tissue gene expression favoring increased lipid storage

  • Combined, these changes upon late eating may increase obesity risk in humans

Summary

Late eating has been linked to obesity risk. It is unclear whether this is caused by changes in hunger and appetite, energy expenditure, or both, and whether molecular pathways in adipose tissues are involved. Therefore, we conducted a randomized, controlled, crossover trial (ClinicalTrials.gov NCT02298790) to determine the effects of late versus early eating while rigorously controlling for nutrient intake, physical activity, sleep, and light exposure. Late eating increased hunger (p < 0.0001) and altered appetite-regulating hormones, increasing waketime and 24-h ghrelin:leptin ratio (p < 0.0001 and p = 0.006, respectively). Furthermore, late eating decreased waketime energy expenditure (p = 0.002) and 24-h core body temperature (p = 0.019). Adipose tissue gene expression analyses showed that late eating altered pathways involved in lipid metabolism, e.g., p38 MAPK signaling, TGF-β signaling, modulation of receptor tyrosine kinases, and autophagy, in a direction consistent with decreased lipolysis/increased adipogenesis. These findings show converging mechanisms by which late eating may result in positive energy balance and increased obesity risk.

Keywords

meal timing
late eating
early eating
energy expenditure
energy intake
hunger
adipose
gene expression
leptin
ghrelin

Data and code availability

  • FAIR Standards Data Availability: In accordance with MIAME and MINSEQE standards, raw data files (FASTQ, IDAT) used for the analysis of gene expression data in this paper were uploaded to the public data repository Gene Expression Omnibus (GEO). Data can be reached at GEO: GSE190168.

  • All other data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials, see Data S1.

  • As per the NIH Policy on Data Sharing, we will make the datasets available to other investigators following publication of the final study results. These datasets will not contain identifying information per the regulations outlined in HIPPA. Per standard Partners HealthCare System policies, we will require from any investigator or entity requesting the data a data-sharing agreement that provides for: (i) a commitment to using the data only for research purposes and not to identify any individual participant; (ii) a commitment to securing the data using appropriate computer technology; and (iii) a commitment to destroying or returning the data after analyses are completed.

  • This paper does not report original code.

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