Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety

Abstract

Supplementary key words triglycerides • nutrition • lipolysis and fatty acid metabolism • diet and dietary lipids • fatty acid • insulin resistance • inflammation • hormones • glucose According to the Centers for Disease Control and Prevention, one in three US adults sleeps fewer than 7 h per night, increasing their risk of obesity and for risk of developing CVD, type 2 diabetes, and earlier mortality, among other comorbidities (1-4). The mechanisms by which chronic insufficient sleep increases cardiometabolic disease risk are poorly understood, but results from carefully controlled laboratory studies demonstrate that sleep restriction simultaneously increases orexigenic hormonal signaling and impairs glucose metabolic functioning (5, 6). Furthermore, there is mounting evidence that adipocyte insulin sensitivity and function are impaired by sleep restriction resulting in aberrantly elevated overnight and early morning NEFAs (7-10). Adipocytes are a key integrator of systemic metabolism, absorbing and storing excess energy postprandially and releasing stored fatty acids as needed to meet the energy requirements of the body (11). Adipocytes respond to the postprandial increase in insulin by suppressing intracellular TG lipolysis and by increasing extracellular lipolysis by transporting LPL from intracellular vesicles to the surface Abstract Chronic sleep restriction, or inadequate sleep, is associated with increased risk of cardiometabolic disease. Laboratory studies demonstrate that sleep restriction causes impaired whole-body insulin sensitivity and glucose disposal. Evidence suggests that inadequate sleep also impairs adipose tissue insulin sensitivity and the NEFA rebound during intravenous glucose tolerance tests, yet no studies have examined the effects of sleep restriction on high-fat meal lipemia. We assessed the effect of 5 h time in bed (TIB) per night for four consecutive nights on postprandial lipemia following a standardized high-fat dinner (HFD). Furthermore, we assessed whether one night of recovery sleep (10 h TIB) was sufficient to restore postprandial metabolism to baseline. We found that postprandial triglyceride (TG) area under the curve was suppressed by sleep restriction (P = 0.01), but returned to baseline values following one night of recovery. Sleep restriction decreased NEFAs throughout the HFD (P = 0.02) and NEFAs remained suppressed in the recovery condition (P = 0.04). Sleep restriction also decreased participant-reported fullness or satiety (P = 0.03), and decreased postprandial interleukin-6 (P < 0.01). Our findings indicate that four nights of 5 h TIB per night impair postprandial lipemia and that one night of recovery sleep may be adequate for recovery of TG metabolism, but not for markers of adipocyte function.

Changes in Subjective Motivation and Effort During Sleep Restriction Moderate Interindividual Differences in Attentional Performance in Healthy Young Men

“…Participants consumed three meals per day (breakfast at 09:05, lunch at 12:05, and dinner at 18:05). Meals did not contain caffeine or alcohol (see Ness et al 51 for further details).…”

Impact of sleep deprivation and high-fat feeding on insulin sensitivity and beta cell function in dogs

“…For example, the current study assessed Adipo-IR after one night of total sleep deprivation. In contrast, results from human studies suggest chronic partial sleep loss impairs adipose tissue function as indicated by impaired insulin signalling [5], increased nocturnal NEFA [4] and impaired NEFA rebound [27]. Therefore, a longer duration of insufficient sleep may be necessary to induce alterations in Adipo-IR.…”

Plasma Free Fatty Acid Concentration as a Modifiable Risk Factor for Metabolic Disease

“…As discussed above in relation to weight loss studies, it is important to be cautious when interpreting studies that did not employ a control group. Two studies of sleep deprivation were reported (5 h vs. 10 h of ‘time in bed’ per night) using data from the same study participants [ 106 , 107 ]; participants were studied before, during, and after this reduction in sleep to 5 h per night, yet no control group was studied over the same timeframe. In one of these studies, plasma FFA concentration was surprisingly reduced after four nights of sleep restriction and remained reduced below baseline after restoration of sleeping patterns [ 107 ].…”