Postprandial Metabolic Profiles Following Meals and Snacks Eaten during Simulated Night and Day Shift Work

Abstract

Shift workers are known to have an increased risk of developing cardiovascular disease (CVD) compared with day workers. An important factor contributing to this increased risk could be the increased incidence of postprandial metabolic risk factors for CVD among shift workers, as a consequence of the maladaptation of endogenous circadian rhythms to abrupt changes in shift times. We have previously shown that both simulated and real shift workers showed relatively impaired glucose and lipid tolerance if a single test meal was consumed between 00:00-02:00 h (night shift) compared with 12:00-14:00 h (day shift). The objective of the present study was to extend these observations to compare the cumulative metabolic effect of consecutive snacks/meals, as might normally be consumed throughout a period of night or day shift work. In a randomized crossover study, eight healthy nonobese men (20-33 yrs, BMI 20-25kg/m2) consumed a combination of two meals and a snack on two occasions following a standardized prestudy meal, simulating night and day shift working (total energy 2500 kcal: 40% fat, 50% carbohydrate, 10% protein). Meals were consumed at 01:00/ 13:00 h and 07:00/19:00h, and the snack at 04:00/16:00 h. Blood was taken after an overnight fast, and for 8 h following the first meal on each occasion, for the measurement of glucose, insulin, triacylglycerol (TAG), and nonesterified fatty acids (NEFA). RM-ANOVA (factors time and shift) showed a significant effect of shift for plasma TAG, with higher levels on simulated night compared to day shift (p < 0.05). There was a trend toward an effect of shift for plasma glucose, with higher plasma glucose at night (p = 0.08), and there was a time-shift interaction for plasma insulin levels (p < 0.01). NEFA levels were unaffected by shift. Inspection of the area under the plasma response curve (AUC) following each meal and snack revealed that the differences in lipid tolerance occurred throughout the study, with greatest differences occurring following the mid-shift snack. In contrast, glucose tolerance was relatively impaired following the first night-time meal, with no differences observed following the second meal. Plasma insulin levels were significantly lower following the first meal (p < 0.05), but significantly higher following the second meal (p < 0.01) on the simulated night shift. These findings confirm our previous observations of raised postprandial TAG and glucose at night, and show that sequential meal ingestion has a more pronounced effect on subsequent lipid than carbohydrate tolerance.

Is the timing of caloric intake associated with variation in diet-induced thermogenesis and in the metabolic pattern? A randomized cross-over study

“…Therefore, both the circadian variation in catecholamine 277 concentrations and in insulin sensitivity might contribute to the evening reduction of DIT. Consistent with the 278 reported reduced insulin sensitivity at evening, we found lower glucose/insulin AUCs in the morning and 279 delayed and larger increases in the concentrations of glucose and insulin in the evening (Figures 2-3, Table 2SI,afternoon [2], and an increased activity of lipoprotein lipase during the daytime [27]. The circadian activity of 283 clock target genes in adipocytes may impact on lipid breakdown and adipokine function, by regulating FFA 284 mobilization from adipose tissue, thus acting on energy homeostasis and metabolic processes [32][33].…”

“…Other explanations for the reduced evening post-prandial thermic and metabolic answers may 268 be the slower evening gastric emptying, with increased efficacy of dietary carbohydrates absorption [5][6], and 269 the reported decrement in insulin sensitivity as evening progresses [3]. Possible contributors to the daily 270 variations in insulin secretion, with higher morning beta-cell function and action, could be the circadian 271 fluctuation in the concentrations of cortisol, ACTH, glucagon-like peptide 1, glucose-dependent insulinotropic 272 polypeptide, as well as in the meal-induced glucagon responses, showing a delayed peak after evening meals 273 [2][3][27][28][29]. Insulin resistance may determine a decreased thermic effect of glucose because of the diminished 274 insulin-mediated glucose uptake and metabolism by skeletal muscle that results in diminished glucose-induced 275 thermogenesis [8,30].…”

“…Circadian 333 misalignment has adverse metabolic and cardiovascular consequences [4,46]. Examples of chronic conditions 334 of this phenomenon are shift work and sleep deprivation, both conditions being associated with an increased 335 risk of obesity, metabolic syndrome and cardiovascular diseases [27,31,33]. 336…”

Assessment of lipid, hepatic, and thyroid parameters with serum perfluorooctanoate (PFOA) concentrations in fluorochemical production workers

“…Countering this possible hypothesis is the fact that blood glucose, also requiring a fasting sample, was not associated with PFOA at any site. However, hyperglycemia has not been consistently associated with night shift workers (Al-Naimi et al 2004;Karlsson et al 2003). Also, the association between serum triglycerides and PFOA was not observed at the Cottage Grove site which had both production and non-production workers.…”

“…It can also be hypothesized that the associations observed for serum triglycerides and PFOA might be the consequence of the non-adherence to fasting requirements by some shift production workers and/or the effect of postprandial metabolic responses in shift workers. Several studies have indicated postprandial serum triglyceride levels are higher among night shift workers than day workers (Al-Naimi et al 2004;Morgan et al 1998;Karlsson et al 2001;Lund et al 2001). If a subset of subjects (i.e., production workers with higher PFOA serum concentrations) who worked night shift were less likely to adhere to the fasting requirements and/or have postprandial metabolic profiles similar to other night shift workers, then a non-causal positive association between PFOA concentrations and serum triglycerides could be observed when all subjects are included in the analysis.…”