Postprandial hormone and metabolic responses in simulated shift work

School of Biological Sciences, University of Surrey, Guildford, UK.
Journal of Endocrinology (Impact Factor: 3.72). 11/1996; 151(2):259-67. DOI: 10.1677/joe.0.1510259
Source: PubMed


This study was designed to investigate postprandial responses to a mixed meal in simulated shift work conditions. Nine normal healthy subjects (six males and three females) were studied on two occasions at the same clock time (1330 h) after consuming test meals, first in their normal environment and secondly after a 9 h phase advance (body clock time 2230 h). Plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), triacylglycerol (TAG) and non-esterified fatty acids (NEFAs) were determined at intervals for 6 h after each test meal. Postprandial plasma glucose, insulin, GIP and GLP-1 profiles were evaluated by calculating areas under the curve (AUC) for the first 2 h and the last 4 h of the sampling together with total AUC. Significantly higher postprandial glucose responses (total AUC) were observed after the phase shift than before (AUC 0-360 min, 2.01 (1.51-2.19) vs 1.79 (1.56-2.04) mmol/l.min; P < 0.02; mean (range)). No significant difference was observed when the first 2 h of each response was compared, but significantly higher glucose levels were observed in the last 4 h of the study after the phase shift than before (AUC 120-360 min, 1.32 (1.08-1.42) vs 1.16 (1.00-1.28) mmol/l.min; P < 0.05). Similar results were obtained for insulin (AUC 0-360 min, 81.72 (30.75-124.97) vs 58.98 (28.03-92.57) pmol/l.min; P < 0.01; AUC 120-360 min, 40.73 (16.20-65.25) vs 25.71 (14.25-37.33) pmol/l.min; P < 0.02). No differences were observed in postprandial plasma GIP and GLP-1 responses before and after the phase shift. Postprandial circulating lipid levels were affected by phase shifting. Peak plasma TAG levels occurred 5 h postprandially before the phase shift. Postprandial rises in plasma TAG were significantly delayed after the phase shift and TAG levels continued to rise throughout the study. Plasma postprandial NEFA levels fell during the first 3 h both before and after the phase shift. Their rate of return to basal levels was significantly delayed after the phase shift compared with before. This study demonstrates that a simulated phase shift can significantly alter pancreatic B-cell responses and postprandial glucose and lipid metabolism.

Download full-text


Available from: Linda Morgan, Jul 09, 2014
  • Source
    • "The most recognized cause of circadian misalignment is jet lag after crossing multiple time zones, although night-shift work and early school or work times are other situations in which individuals can experience circadian misalignment. In laboratory studies that experimentally imposed severe acute circadian misalignment, healthy participants showed adverse metabolic responses that are risk factors for cardiovascular disease and type 2 diabetes [1] [8] [9]. When experienced chronically like in night-shift work, circadian misalignment increases the risk of a number of diseases , including cancer [13] [14] [15] [16] [17] [18]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Efficient treatments to phase-advance human circadian rhythms are needed to attenuate circadian misalignment and the associated negative health outcomes that accompany early-morning shift work, early school start times, jet lag, and delayed sleep phase disorder. This study compared three morning bright-light exposure patterns from a single light box (to mimic home treatment) in combination with afternoon melatonin. Methods: Fifty adults (27 males) aged 25.9 ± 5.1 years participated. Sleep/dark was advanced 1 h/day for three treatment days. Participants took 0.5 mg of melatonin 5 h before the baseline bedtime on treatment day 1, and an hour earlier each treatment day. They were exposed to one of three bright-light (~5000 lux) patterns upon waking each morning: four 30-min exposures separated by 30 min of room light (2-h group), four 15-min exposures separated by 45 min of room light (1-h group), and one 30-min exposure (0.5-h group). Dim-light melatonin onsets (DLMOs) before and after treatment determined the phase advance. Results: Compared to the 2-h group (phase shift = 2.4 ± 0.8 h), smaller phase-advance shifts were seen in the 1-h (1.7 ± 0.7 h) and 0.5-h (1.8 ± 0.8 h) groups. The 2-h pattern produced the largest phase advance; however, the single 30-min bright-light exposure was as effective as 1 h of bright light spread over 3.25 h, and it produced 75% of the phase shift observed with 2 h of bright light. Conclusions: A 30-min morning bright-light exposure with afternoon melatonin is an efficient treatment to phase-advance human circadian rhythms.
    Sleep Medicine 12/2014; 16(2). DOI:10.1016/j.sleep.2014.12.004 · 3.15 Impact Factor
  • Source
    • "Interestingly, the postprandial response in such protocols is altered by the preceding diet. In comparable experiments, the exaggerated postprandial response following a test meal in shifted subjects was reduced for glucose and insulin but increased for TAG following a low-fat pre-meal( 150 ) rather than a high-fat pre-meal( 151 ). Furthermore, there are reported sex differences in postprandial response, with a more pronounced elevation of TAG in the first night of a simulated night shift in men than in women( 90 ). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Circadian rhythms act to optimise many aspects of our biology and thereby ensure that physiological processes are occurring at the most appropriate time. The importance of this temporal control is demonstrated by the strong associations between circadian disruption, morbidity and disease pathology. There is now a wealth of evidence linking the circadian timing system to metabolic physiology and nutrition. Relationships between these processes are often reciprocal, such that the circadian system drives temporal changes in metabolic pathways and changes in metabolic/nutritional status alter core molecular components of circadian rhythms. Examples of metabolic rhythms include daily changes in glucose homeostasis, insulin sensitivity and postprandial response. Time of day alters lipid and glucose profiles following individual meals whereas, over a longer time scale, meal timing regulates adiposity and body weight; these changes may occur via the ability of timed feeding to synchronise local circadian rhythms in metabolically active tissues. Much of the work in this research field has utilised animal and cellular model systems. Although these studies are highly informative and persuasive, there is a largely unmet need to translate basic biological data to humans. The results of such translational studies may open up possibilities for using timed dietary manipulations to help restore circadian synchrony and downstream physiology. Given the large number of individuals with disrupted rhythms due to, for example, shift work, jet-lag, sleep disorders and blindness, such dietary manipulations could provide widespread improvements in health and also economic performance.
    Nutrition Research Reviews 03/2014; 27(1):1-12. DOI:10.1017/S0954422414000055 · 3.91 Impact Factor
  • Source
    • "Increased adiposity and altered glucose metabolism create a positive feedback loop that results in more profound adiposity (i.e., obesity) and poorer glucose metabolism that can culminate in diabetes or untimely death. Impaired glucose tolerance, which is thought to be a precursor to T ype 2 Diabetes, was observed in shift workers starting a new rotation (Lund et al., 2001) and in subjects who experienced simulated shift work (Hampton et al., 1996). Similarly, in addition to increased serum glucose, Scheer and colleagues observed decreased leptin, increased insulin, decreased sleep efficiency, increased blood pressure, and a change in the phase of the cortisol rhythm in people that were subjected to a seven day circadian disruption protocol meant to resemble shift work (Scheer et al., 2009). "
    [Show abstract] [Hide abstract]
    ABSTRACT: This review consolidates research employing human correlational and experimental work across brain and body with experimental animal models to provide a more complete representation of how circadian rhythms influence almost all aspects of life. In doing so, we will cover the morphological and biochemical pathways responsible for rhythm generation as well as interactions between these systems and others (e.g., stress, feeding, reproduction). The effects of circadian disruption on the health of humans, including time of day effects, cognitive sequelae, dementia, Alzheimer's disease, diet, obesity, food preferences, mood disorders, and cancer will also be discussed. Subsequently, experimental support for these largely correlational human studies conducted in non-human animal models will be described.
    Neuroscience & Biobehavioral Reviews 01/2014; 40C. DOI:10.1016/j.neubiorev.2014.01.007 · 8.80 Impact Factor
Show more