Metabolic Effects of Late Dinner in Healthy Volunteers—A Randomized Crossover Clinical Trial

Author:

Gu Chenjuan1ORCID,Brereton Nga2,Schweitzer Amy2,Cotter Matthew3,Duan Daisy4,Børsheim Elisabet356,Wolfe Robert R56,Pham Luu V1,Polotsky Vsevolod Y1,Jun Jonathan C1ORCID

Affiliation:

1. Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland

2. Institute for Clinical and Translational Research, Johns Hopkins University, Baltimore, Maryland

3. Arkansas Children’s Nutrition Center, Arkansas Children’s Research Institute, Little Rock, Arkansas

4. Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Johns Hopkins University, Baltimore, Maryland

5. Department of Pediatrics, The University of Arkansas for Medical Sciences, Little Rock, Arkansas

6. Department of Geriatrics, Center for Translational Research in Aging and Longevity, The University of Arkansas for Medical Sciences, Little Rock, Arkansas

Abstract

AbstractContextConsuming calories later in the day is associated with obesity and metabolic syndrome. We hypothesized that eating a late dinner alters substrate metabolism during sleep in a manner that promotes obesity.ObjectiveThe objective of this work is to examine the impact of late dinner on nocturnal metabolism in healthy volunteers.Design and SettingThis is a randomized crossover trial of late dinner (LD, 22:00) vs routine dinner (RD, 18:00), with a fixed sleep period (23:00-07:00) in a laboratory setting.ParticipantsParticipants comprised 20 healthy volunteers (10 male, 10 female), age 26.0 ± 0.6 years, body mass index 23.2 ± 0.7 kg/m2, accustomed to a bedtime between 22:00 and 01:00.InterventionsAn isocaloric macronutrient diet was administered on both visits. Dinner (35% daily kcal, 50% carbohydrate, 35% fat) with an oral lipid tracer ([2H31] palmitate, 15 mg/kg) was given at 18:00 with RD and 22:00 with LD.Main Outcome MeasuresMeasurements included nocturnal and next-morning hourly plasma glucose, insulin, triglycerides, free fatty acids (FFAs), cortisol, dietary fatty acid oxidation, and overnight polysomnography.ResultsLD caused a 4-hour shift in the postprandial period, overlapping with the sleep phase. Independent of this shift, the postprandial period following LD was characterized by higher glucose, a triglyceride peak delay, and lower FFA and dietary fatty acid oxidation. LD did not affect sleep architecture, but increased plasma cortisol. These metabolic changes were most pronounced in habitual earlier sleepers determined by actigraphy monitoring.ConclusionLD induces nocturnal glucose intolerance, and reduces fatty acid oxidation and mobilization, particularly in earlier sleepers. These effects might promote obesity if they recur chronically.

Funder

National Institutes of Health

American Heart Association

Publisher

The Endocrine Society

Subject

Biochemistry (medical),Clinical Biochemistry,Endocrinology,Biochemistry,Endocrinology, Diabetes and Metabolism

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