Sleep restriction increases free fatty acids in healthy men

Abstract

Aims/hypothesis Sleep loss is associated with insulin resistance and an increased risk for type 2 diabetes, yet underlying mechanisms are not understood. Elevation of circulating non-esterified (i.e. free) fatty acid (NEFA) concentrations can lead to insulin resistance and plays a central role in the development of metabolic diseases. Circulating NEFA in healthy individuals shows a marked diurnal variation with maximum levels occurring at night, yet the impact of sleep loss on NEFA levels across the 24 h cycle remains unknown. We hypothesised that sleep restriction would alter hormones that are known to stimulate lipolysis and lead to an increase in NEFA levels. Methods We studied 19 healthy young men under controlled laboratory conditions with four consecutive nights of 8.5 h in bed (normal sleep) and 4.5 h in bed (sleep restriction) in randomised order. The 24 h blood profiles of NEFA, growth hormone (GH), noradrenaline (norepinephrine), cortisol, glucose and insulin were simultaneously assessed. Insulin sensitivity was estimated by a frequently sampled intravenous glucose tolerance test. Results Sleep restriction relative to normal sleep resulted in increased NEFA levels during the nocturnal and early-morning hours. The elevation in NEFA was related to prolonged nocturnal GH secretion and higher early-morning noradrenaline levels. Insulin sensitivity was decreased after sleep restriction and the reduction in insulin sensitivity was correlated with the increase in nocturnal NEFA levels. Conclusions/interpretation Sleep restriction in healthy men results in increased nocturnal and early-morning NEFA levels, which may partly contribute to insulin resistance and the elevated diabetes risk associated with sleep loss.

Therapeutic Methods Against Insulin Resistance

“…The hypothalamic parenchyma is constituted by nuclear groups (about 11 major nuclei) intermingled with bands of unmyelinated and myelinated fibers, especially from the medial temporal lobes [22,23] and prefrontal limbic areas [5,24]. Both of them related with sleep disorders [25,26] and stressful impulses on the hypothalamic nuclei [5,[27][28][29][30][31][32]. Figure 1 represents the hippocampus, which is located in the medial temporal lobes and is constituted by dentate gyrus and the cornu Ammon with their CA1 to CA4 subdivisions [2,13,33,34].…”

“…Finally, clinical evidence suggests that chronic stress and sleep disorders or loss may be related with increased fatty acids levels, which may partly contribute to insulin resistance [25,26], due, probably, to a dysfunction of hypothalamus and limbic system caused by ischemia [5,22,29]. The clonazepam can improve or abort these sleep disorders and slow or dampen stressful stimuli [22,32].…”

Elevated nocturnal NEFA are an early signal for hyperinsulinaemic compensation during diet-induced insulin resistance in dogs

“…In striking contrast, nocturnal NEFA are markedly elevated after high-fat feeding [7]. A normal nocturnal rise in NEFA has been demonstrated in human volunteers [8], and this nocturnal increase is elevated during sleep-restriction-induced insulin resistance [9]. What is unknown is whether the nocturnal increase in NEFA that occurs in an insulin-resistant state is an initial signal for hyperinsulinaemic compensation in the face of insulin resistance.…”

Does higher energy intake explain weight gain and increased metabolic risks among shift workers?

“…The exact mechanisms for these associations are not firmly established (5). Short-term sleep restriction is known to induce insulin resistance and, for example, disturbances in fat metabolism (6), and shift workers are known to suffer from sleep loss. It is plausible that lifestyle factors related to shift work play a role as well.…”