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

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 NCT0...

Full description

Saved in:
Bibliographic Details
Published inCell metabolism Vol. 34; no. 10; pp. 1486 - 1498.e7
Main Authors Vujović, Nina, Piron, Matthew J, Qian, Jingyi, Chellappa, Sarah L, Nedeltcheva, Arlet, Barr, David, Heng, Su Wei, Kerlin, Kayla, Srivastav, Suhina, Wang, Wei, Shoji, Brent, Garaulet, Marta, Brady, Matthew J, Scheer, Frank A J L
Format Journal Article
LanguageEnglish
Published United States 04.10.2022
Subjects
Adult
Appetite
Eating - physiology
Energy Intake
Energy Metabolism - physiology
Ghrelin - metabolism
Humans
Hunger - physiology
Leptin - metabolism
Metabolic Networks and Pathways
Obesity - metabolism
Overweight
p38 Mitogen-Activated Protein Kinases - metabolism
Transforming Growth Factor beta - metabolism
Tyrosine - metabolism
energy intake
ghrelin
late eating
adipose
early eating
energy expenditure
meal timing
leptin
gene expression
hunger
Online AccessGet full text

Cover

More Information
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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Undefined-3
N.V., M.J.P., M.J.B. and F.A.J.L.S. wrote the manuscript, with editorial input from M.G., J.Q., S.L.C., A.N., D.B., K.K.M., S.H., S.S., W.W., and B.S.; original draft prepared by N.V.
F.A.J.L.S. acquired funding.
M.J.P. and M.J.B. developed the study design and methodology for molecular analyses.
N.V., J.Q., S.L.C., A.N., D.B., and F.A.J.L.S. coordinated research activity planning and execution.
K.K.M., S.H., S.S. recruited study participants and collected data.
N.V., M.J.P., S.L.C. and J.Q. were responsible for visualization and presentation of data.
F.A.J.L.S. supervised research activity.
N.V., M.J.P. and W.W. performed statistical analyses.
F.A.J.L.S, M.J.B. and M.G. conceptualized the study (i.e., were involved in formulation/evolution of overarching research goals and aims).
AUTHOR CONTRIBUTIONS
F.A.J.L.S, D.B., A.N., N.V. and B.S. developed the study design and methodology for human inpatient experiments.
Lead contact
ISSN:1550-4131
1932-7420
DOI:10.1016/j.cmet.2022.09.007