Late Dinners Increase Blood Glucose, Could Promote Obesity
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Consuming calories later in the day is associated with obesity and metabolic syndrome. This study hypothesized that eating a late dinner alters substrate metabolism during sleep in a manner that promotes obesity.

The objective of this study was to examine the impact of late dinner on nocturnal metabolism in healthy volunteers. This was a randomized crossover trial of late dinner versus routine dinner, with a fixed sleep period in a laboratory setting.

20 healthy volunteers (10 males, 10 females), aged 26.0 ± 0.6 years, BMI 23.2 ± 0.7 kg/m2, accustomed to a bedtime between 22:00-01:00. An 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 on RD and 22:00 on LD.

Nocturnal and next-morning hourly plasma glucose, insulin, triglycerides, free fatty acids (FFAs), cortisol, dietary fatty acid oxidation, and overnight polysomnography were assessed.

Results: LD 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.

Conclusively, LD induces nocturnal glucose intolerance, and reduces fatty acid oxidation and mobilization, particularly in earlier sleepers. These effects might promote obesity if they recur chronically.