Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [array]

Late eating has been linked to obesity risk. It is not clear whether this is caused by changes in hunger and appetite, energy expenditure or both, nor what molecular pathways in adipose tissues are involved. We conducted a randomized crossover trial to determine the effects of late vs. early meal schedule on the above measures while rigorously controlling for nutrient intake, fasting duration, light exposure, physical activity and sleep opportunity. Late mealtimes doubled the odds of participants reporting hunger (p<0.0001), increased 24-h ghrelin:leptin ratio (p<0.0001) and decreased waketime energy expenditure (p=0.002). Adipose biopsy directional gene expression analyses showed alterations of several pathways attributed to late mealtimes: TGF-β signaling, lipid metabolism, p38 MAPK signaling, modulation of receptor tyrosine kinases, and autophagy, indicating decreased lipolysis/increased lipid synthesis, particularly for phospholipids and membrane-bound lipids. These findings may help develop evidence-based approaches for using appropriate meal timing to prevent and/or treat obesity. Total RNA obtained from SubQ adipose biopsy under early or late eating protocols.